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217 Cards in this Set

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Features of Lambert Eaton syndrome
increased muscle strength after repetitions
limb girdle weakness
hyporeflexia
Autonomic: dry mouth, impotence, difficulty micturating
NOT a feature = ophthalmoplegia and ptosis
Pathophysiology of Lambert Eaton syndrome
Ab directed against pre-synaptic voltage gated calcium channels in peripheral nervous system
Classic triad of Wernicke's encephalopathy
ataxia
confusion
ophthalmoplegia
nystagmus
NOT confabulation (in Korsakoff's)
Features of Lewy body dementia
visual hallucinations
progressive cognitive decline
Parkinsonism
sensitive to neuroleptics (haloperidol, chlorpromazine)
Physiology of neuroleptic malignant syndrome
massive dopamine blockade
Visual examination in craniopharyngioma
bitemporal hemianopia, lower visual fields affected more significantly
Visual examination in pituitary tumor
bitemporal hemianopia, superior visual fields affected more significantly
Features of parietal lobe lesions
astereoagnosia (inability to tell things by touching them)
hemi-neglect
apraxia
sensory inattention
inferior homonymous quadrantanopia
Gerstmann's syndrome = L-R disorientation, alexia, acalculia, finger agnosia
Features of occiptal lobe lesions
homonymous hemianopia
cortical blindness
visual agnosia
Features of temporal lobe lesions
Wernicke's aphasia
superior homonymous hemianopia
auditory agnosia
difficulty recognising faces (prosopagnosia)
Features of frontal lobe lesions
Broca's (expressive) aphasia
disinhibition
preservation
anosmia
inability to generate a list
Features of normal pressure hydrocephalus
urinary incontinence
apraxia, gait abnormality (similar to Parkinson's)
dementia
Features that point to diagnosis of motor neuron disease
fasiculations
absence of sensory symptoms
LMN signs in arms
UMN signs in legs
wasting of small hand muscles
T/F Nerve conduction studies are normal in motor neuron disease.
True
Features of neurofibromatosis type 1
Cafe au lait spots
axilalry/groin freckles
peripheral neurofibromas
Lisch nodules
scoliosis
Which chromosome is implicated in neurofibromatosis type 1?
17 (think neurofibromatosis has 17 characters!)
Features of neurofibromatosis type 2
bilateral acoustic neuromas (vestibular schwannoma)
Common side effect of metoclopramide
extra-pyramidal symptoms
Treatment of stroke
rule out hemorrhage, then aspirin
if under 3 hours: thrombolysis with tPA/streotokinase
Features of cluster headache
watery eyes
intense pain and redness around one eye
nasal stuffiness
pain occurs 1-2x per day
ptosis and miosis
Features of Meniere's disease
aural fullness
tinnitus
hearing loss
vertigo lasting min/hours
Features of BPPV
vertigo for a few seconds/min
certain positions
nystagmus
Managment of Meniere's disease
draining
thiazides
Management of BPPV
spontaneous recovery
Epley's and Brant-Daroff maneuveres
surgery
Features of Von Hippel-Lindau disease
cerebellar and retinal hemangiomas, vitreous hemorrhage
renal cysts
adenomas
phaeochromocytoma
Treatment for MS
interferon beta
Treatment of restless leg syndrome
dopamine agonist, eg ropinirole
Pharmacological treatment of Alzheimer's
acetylchoine esterase inhibitors (donepezil) for mild-moderate
NMDAr antagonist (memantine) for moderate-severe
What runs through the cavernous sinus?
CN 3, 4, 5 (V1 & 2, not mandibular), 6
internal carotid artery
SEs of levo-dopa
postural hypotension
psychosis
on-off effect
arrhythmias
dyskinesias
N & V
What is a common infective cause of Guillian Barre syndomre
Campylobacter jejuni
what are the 4 patterns of MS
Relapsing Remitting
Progressive relapsing
Primary progressive
Scondary progressive (initially relapsing then progresses to progresive)
Which HLA is associated with MS
HLA-DR2
What is the aetiology of MS
Genetic - HLA-DR2
Environmental - MS is more common in regions with less sun exposure and less vit D (retain risk of area in which you grew up < 15)
Association with EBV
What questions do you want to ask in a history of MS?
Onset
Initial neurological deficit
Any episodes of spastic paraparesis, hemiparesis or tetraparesis; limb paraesthesiae; reversible visual loss or ocular pain, loss of central visual field (optic neuritis) weakness, incoordination, band sensations around trunk and limbs; lancinating pain, speech impairment, sphincter disturbances, sensory loss, vertigo, gait difficult
Lhermitte's phenomenon (electric shock-like pain radiating down the spine, triggered by neck flexion)
Precipitating factors: heat; infection, fever, pregnancy, exercise Disease pattern and temporal profile
Complications associated with neurological deficit (aspiration pneumonia, UTI, mechanical injuries, limb contractures, pressure areas and painful mm spasms)
Functional level of patient, social and occupational difficulties associated with sexual function
Mood
Fatigue
Family history, patient's place of birth
Pregnancy - 20-30% increase in relapse rate first month after delivery
Different treatments and adverse effects
Examination of patient with MS
Full neurological exam
part. visual examination - ecternal ocular movements, INO, optic atrophy, afferent pupillary defect
Spinal cord signs
bulbar signs
cerebellar signs
cerebral hemisphere signs
MMSE - can lead to cognitive impairment
What is internuclear opthalmaplegia
Disease of conjugate lateral gaze
Weakness of adduction in one eye as a result of damage to the ipsilateral medial longitudinal fasciculus. There is nystagmus in the abducting eye.
When affected eye tries to look contralaterally it cannot adduct
Often bilateral in MS
What are the different MS variants?
Delvis = neuromyelitis optica = episode of optic neuritis and transverse myelitis occuring within a few weeks of one another
Benign MS: RR without major disability for 10 years
Clinical isolated syndrome = single MS episode
Typical locations of MS plaques on MRI
periventricular, corpus callosum, cerebellar peduncles, brainstem, juxt cortical region, dorslateral spinal cord
What are dawson's fingers
periventricular lesions extending superiorly into corpus callosum
What investigations are done in MS
MRI
T2 weighted - hyperintense lesions
gadolinium shows up acute lesions
CSF oligoclonal bands - antibodies depicted as bands on agragose gel
Evoked potentials (visual/auditory/somatosensory) - generated by peripheral stimulation of a sensory organ
Features of MS on MRI
a) Classical lesions perpendicular to ventricles and in corpus callosum—'Dawson's fingers'

b) Lesions tend to be periventricular, whereas in vasculitis they are more peripheral

c) Subcortical U fibres, characteristic of multiple sclerosis

d) Cerebellar (infratentorial) plaque

e) Cortex may show atrophy
Differential diagnosis of MS
SLE
HIV
Sarcoidosis
Spinal or brainstem lesion
Metabolic disorder - Vit B12 deficiency
Coag disorder
Management of MS
Acute relapses - steroids
Underlying disease - Immune modulators: Interferon beta SE: depression, flu like; skin re; LFTs, platelet and WCC reduction; thyroid antibodies; can develop neutralising antibodes (reduce effectiveness of drug); glatiramer acetate; atalizumab
Immunosuppressants:
Methotrexate; Azathioprine
What is the definition of epilepsy?
Chronic condition characterised by 2 or more unprovoked seizures
Seizure = transient neurological dysfunction caused by excessive activity of cortical neurons, resulting in paroxysmal alteration of behaviour and/or EEG changes
What are the risk factors for epilepsy?
Family history
Head injury
Meningitis/encephalitis
MS
Drugs (alcohol, heroin, MJ)
Complex febrile convulsions
Alzheimer's
CVD
What is the difference between simple and complex seizures?
Simple - no LOC
Complex - LOC (alteration of mood, memory, perception)
Do you get LOC in generalised seizures?
Yes
What are automatism and when do you see them?
Brief unconcious behaviours
Chewing, swallowing, lip-smacking, scracthcing, fubling, running, disrobing, prior to LOC followed by distant staring unresponsiveness
What are the different types of generalised seizures that you can get?
Tonic-clonic (grand mal):
Absence
Tonic
Clonic
Myoclonic
Atonic
Describe the features of a tonic clonic seizure
Prodrome: unease or irritability hours to days before the attack (aura sometimes)
Tonic: tonic mm contractions, arm flexion and adduction, leg extension, 'cry' as respiratory mm spasm and air is expelled; 10-30 secs
Clonic: clonus involving violent jerks of face and limbns, tongue biting, incontinence; < 90 secs
Ictal autonomic outpouring (hypertension, tachycardia, hypersalivation, pupilary dilation)
Describe the symptoms felt after a tonic clonic seizure
decreased LOC, flaccid limb and jaw, extensor plantar reflexes, loss of corneal reflexes
headache, confusion, aching mm, sore tongue, amnesia, elevated serum CK lasting hours
What are the features of an absence seizure?
Non convulsive event - unresponsive for 5-10 seconds with arrest of activity, starring, blinking or eye rolling
No memory of event
No postural loss b/e seizure doesn't spread across both hemispheres
Ca is involved
Generaly age of onset 6-7 girls> boys
Remission in 80% by adolescence
20% turn into generalised tonic-clonic seizures
Features of a myoclonic seizure
brief contractions localised to mm groups of one or more extremities or more generalised
age of onset 12-16 years
generally seen in the am
very responsive to therapy
What are the features of an atonic seizure
loss of postural tone leading to drop attack
What type of features are characteristic of partial seizures
Simple vs complex
motor
sensory
autonomic
psychiatric
What is a Jacksonian March?
Symptoms of a seizure start in one location and spread to another
What type of epilepsy is suggested by an aura of fear, olfactory or gustatory hallucinations, visveral or deja vu sensations?
Temporal lobe epilepsy
What type of seizures are suggested by contralateral focal sensory or motor phenomena
Frontoparietal cortex seizures
What can complex partial seizures sometimes resemble?
schizophrenia or psychotic depression
What is a non-epileptic (pseudo) seizure?
Physical manifestation of a psychological disturbance
Normal EEG
Paroxysmal episodes either organic (TIA, syncope, migraine) or psychogenic
Rare to have physical injury, incontinence
Usually occur during the day with other people present
Features include: opisthotonos, rigidity, forced eye closure, irregular exctremity movements, shaking head, pelvic thrust, crying
Outline the common causes of seizures in infancy and early childhood
Febrile
Congenital
Inborn errors of metabolism
perinatal injury
Outline the common causes of seizures in older adults
Cerebral tumours
Neurodegenerative disease
CVD
Outline the common cause of seizures in adolescents
head injury
What is Todd's post-ictal phenomena?
Post-ictal depressed function of the local cortex involved producing focal weakness --> Todd's hemiparesis
Usually seen if seizures are prolonged or recurrent
When should a patient having a seizure be transferred to hospital?
Status epilepticus or multiple seizures
First seizure
Pregnancy or diabetic or injury
What questions should you be thinking about in the management of a first seizure?
Was it actually a seizure?
LOC? What type?
Any secondary injury (i.e. bitten tongue)
Evidence of CNS dysfunction
Precipitating factors
Investigations to be ordered
Should you start an anti-epileptic drug?
What causes seizures?
In patient with known epilepsy
Hypoglycaemia
ETOH excess of withdrawal
Intercurrent infection
Stress
INadequate anticonvulsant therapy
head injury
In non-epileptic
CNS (head injury, brain tumour, CVD, infection, hypertensive encephalopathy,
Endocrine (hypoglycaemia, hyponatraemia, hypocalcaemia, hypomagnesia, uraemia)
Systemic disorder (eclampsia, hypoxia, hypotension, sepsis from renal tract, respiratory or skin infection)
Drug related toxicity and withdrawal (TCAs, cocaine, tramadol, pethidine)
What are the major threats to life involved with seizures?
Hypoxia
aspiration
hyperthermia
Cerebral oedema (if they last > 1 hour)
Immediate management of seizures in hospital?
ABC
Lateral position
O2 mask
If seizure doesn't stop may want to give midazalam or diazepam
Once seizure has stopped immediately follow with phenytoin to prevent recurrence
What investigations should be performed in new onset seizure?
Bloods (FBC, EUC, LFTs, BHCG, CMP, serum glucose, anti convulsant levels)
NB: vigorous seizure alone can cause hyperkalaemia and acidosis
CT head
LP if suspsect SAH or infection
EEG
What is the mechanism of action of phenytoin?
Na channel blocker
Limits the firing frequency of neurons
MOA of Carbemazapine
Na channel blocker (limits the firing frequency of neurons)
Enhances GABA
Activates adenosine receptors which limits the release of excitatory transmitters from the presynaptic terminal e.g., glutamate
MOA sodium valproate
Decreased metabolism of GABA (enhances GABA inhibition)
Trade names for
Phenytoin
Carbemazapine
Sodium valproate
Phenytoin = dilantin
Carbemazapine = tegretol
Sodium valproate = epilim
Which anti-epileptic cannot be used in pregnancy
sodium valproate
Which anticonvulsants are used for generalised epilepsy?
sodium valproate
carbemazapine
Which is the drug of choice for partial epilepsies
Carbemazaepine
IF it fails can use sodium valproate or phenytoin
MOA phenobarbitone
Barbituate (increases Time that GABA channels stay open for
+ decreases release of glutamate from the presynaptic terminal
Which anticonvulsants are used in absence seizures?
Ethosuximide
Sodium valproate
Mechanism of action of ethosuzimide
INcreases seizure threshold
Suppresses characteristic spike and wave pattern in absence seizures
What is status epilepticus?
Seizure that lasts for > 30 mins without spontaneous cessation or recurrent seizures > 30 mins without full return to consciousness inter-ictally (i.e. regaining consciousness in between)
Management of status epilepticus
Protect the airway, always check glucose
Termination of seizure activity
Clonazepam OR diazepam OR midazalam
These are short acting so must follow these with
Phenytoin or sodium valproate
Follow this with ongoing antiepileptic therapy
What questions should be asked to distinguish syncope from a seizure
Time of onset
Precipitating factors
Position
Onset - sudden or gradual
LOC
Ura
Colour
Autonomic effects e.g., diaphoresis (common in syncope)
Duration
Incontinence
Post-ictal confusion
Injury
Automatisms
What do slow background EEG frequencies in the inter-ictal period suggest?
Normal background EEG frequencies
SLow background - underlying insult
NOrmal - primary epilepsy
What is the prognosis of patients with epilepsy?
70% good seizure control and achieve remission
20% need regular medication and may have breakthrough seizures
5-10% poorly controlled
which tumours is located at the cerebellopontine angle?
vesticular schwannoma "acoustic neuroma"
makes up 80-90% of tumours of the CPA
How do patients with vestibular schawnnoma's present?
progressive unilateral or asymmetrical sensorineural hearing loss
Where does the vestibular schwannoma originate from?
CNVIII in internal auditory canal, expanding into bony canal and cerebello-pontine angle
What do bilateral vestibular schwannoma's suggest?
neurofibromatosis type 2
are vestibular schwannoma's benign or malignant?
benign
What clinical features do vestibular schwannoma's have?
CNVIII - hearing loss, tinnitus, dysequilibrium, difficulty walking
V: decreased temperature sensation and face paraesthesias
VII: facial nerve palsy
N+V
Ataxia and raised ICP are late features
How do you manage vestibular schwannoma's?
stereotacic radiosurgery = treatment of choice
surgery if > 3cm, brainstem compression, edema, hydrocephalus
RF for vestibaular schwannoma's?
neurofibromatosis type 2
exposure to loud noice
childhood exposure to low dose radiation
parathyroid adenoma
How can pituitary adenomas present?
Mass effects: headache, bitemporal hemianopis, CN III, IV< V1, V2, VI palsy
endocrine effects: can be functional or non-functional
Pituitary apoplexy = sudden expansion of mass due to haemorrhage or necrosis
- abrupt onset HA, visual disturbances, ophthalmoplegia, reduced mental status, panhypopituitarism
CSF rhinorrhea and seizures
signs and symptoms of SAH (rare)
In what order will a compressive pituiary adenoma ffect the endocrine hormones that is secretes?
"Go Look For The Adenoma Please"
GH
LH
FSH
TSH
ACTH
Prolactin
How does hyperprolactinaemia
present?
infertility
amenorrhea
galactorrhea
decreased libido
What are the DDx if you spot a ring enhancing lesion on CT with contrast?
Most common causes =
mets
abscess
glioblastoma
How might a tumour in the cerebral hemisphere present?
Raised ICP
Progressive neurological deficits specific to site of lesion (usually subacute onset)
Frontal: personality change, apathy, impaired intellect
Parietal: contralateral homonymous hemianopia, cortical sensory loss and motor deficit
Seizures - typically focal
HOw might a cerebellar tumour present?
ataxia ipsilateral to lesion
vertigo, N/V
impaired articular of speech, respiratory movements, motor learning
What is the most common brain tumour seen clinically? Mets or primary?
Mets
what are the most common sites making cerebral mets?
lungs, breast
can also be kidney, colorectal,
thyroid, stomach, prostate, testis, melanoma
What is the ideal imaging study used for brain mets?
contrast enhanced MRI
What radiologic features can differentiate brain mets from other CNS lesions?
multiple lesions
localisation at the junction of grey and white matter
circumscribed margins
large amounts of vasogenic oedema compared to the size of the lesion
usually ring enhancing
what is the prognosis of someone with brain mets?
median survival without treatment once symptomatic is 1 month, with optimal treatment 6-9 months but varies depending on primary
What is the most common primary intra-axial brain tumour?
astrocytoma
4 grades including low grade/diffuse and glioblastoma multiforme
Where is the most common place to find an astrocytoma?
cerebral hemipsheres
then
cerebellum, brainstem, spinal cord
Treatment options for astrocytomas?
surgical resection (usually too large)
radiation
chemo if tumour progression
Are meningioma's benign or malignant?
Mostly benign (1% malignant)
What cell type do meningioma's arise from
arachnoid cells
What features do mengiomas usually present with?
majority are asymptomatic
if over hemispheres can present with seizures, progressive hemiparesis
If at skull base can present with cranial neuropathies
Which brain tumours are contrast enhancing?
Meningioma
Glioblastoma multiforme
Mets
Vestibular schwannoma
oligodendrogiloma show some contrast enhancement
Which brain tumours are not contrast enhancing?
astrocytoma
oligodendroglioma - some show contrast enhancement
Treatment of meningioma?
surgery = treatment of choice if symptomatic or progression on sequential imaging
Which brain tumours have the best survival rate?
meningiomas (mostly benign)
Oligodendroglimoa - medial surval 16 years - most eventually progress to malignancy
Which brain tumour often causes hyperostosis of adjacent bone, often calcified
Meningioma
What symptom/s occur with distortion of the upper brainstem cause?
Decreased level of consciousness
What symptoms occur with compression of the medulla (e.g. when cerebellar tonsils herniate caudally through the foreamen magnum)
impaired consciousness, respiratory depression, bradycardia, decerebrate posturing and death.
Treatment for pituitary apoplexy?
corticosteroids STAT
+/- surgical decompression
Treatment for prolactinoma?
Dopamine agonists (bromocriptine)
Treatment for acromegaly
somatostatin analogue (octreotide) +/- bromocriptine
What drug inhibits cortisol production?
ketaconazole
What is the most common location for carotid artery stenosis
Near the common carotid bifurcation into internal and external carotids
How may carotid artery stenosis present?
TIA or stroke OR
Retinal insufficiency or infarct due to emboli occluding central retinal artery or branches permamently or temporarily (amaurosis fugax)
MCA occlusive symptoms
At what level of occulsion does carotid artery stenosis require an endarterectomy or stenting
> 70% stenosis and symptomatic
What investigations should be done in someone with carotid artery stenosis
FBC, coags
Fundoscopy (cholesterol emboli in retinal vessels = HOllenhorst plaques)
carotid duplex doppler US - size of lumen and flow velocity - least accurate
Angiogram = gold standard but high risk of stroke 1/200
MRA: safter than angiogram but may overestimate stenosis
Pathophysiology of TIAs
Emboli or
In situ thrombosis of an intracranial vessel
What are we worried about in someone whose just had a TIA?
It is an independent RF for a stroke within the next 7 days
What are the 3 causes of ischaemic infarct
Arteriogenic emobolisation
Cardiogenic embolisation
Large vessel thrombus
What is a lacunar infarct?
Which areas do they occur
Occlusion of a small artery branching off from the MCA into deep grey and white matter
Usually in the basal ganglia, thalamus, posterior limb internal capsule
What are some features of a lacunar infarct?
Pure motor hemiparesis: contralateral arm, leg, face
pure sensory loss: hemisensory loss (usually thalamic)
ataxix hemiparesis: ipsilateral ataxia and leg paresis
dysarthria-clumsy hand syndrome: dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness
Risk factors for a lacunar infarct
age
HTN
Most common causes of intracerebral haemorrhage
HTN
Trauma
Bleeding diatheses
Amyloid angiopathy
Vascular malformations
Drugs (cocaine and amphetamines)
Tumours
What are the mechanisms of brain injury in ICH
Mechanical injury secondary to expanding clot
Raised intracranial pressure
Herniation secondary to raised ICP
What is the different in Sx between haemorrhage and SAH, ischaemic stroke
Haemorrhage - the sx begin gradually and form over a few hours, they do not begin abruptly and are not maximal at onset
cf. ischaemic and SAH
Apart from Sx related to the location of the ICH what other features can they have?
Headache - traction on meningeal pain fibres or blood in CSF
Seizures
Stupor/coma
- if stupor is due to involvement of reticulating activating system then may have good recovery otherwise this is an ominous sign
What is the main cause of SAH?
Trauma (most common)
Rupture of arterial aneurysms (75-80%)
idiopathic (14-22%)
AVMs (5%)
coagulopathies, vasculitidies, tumours
What is the classic symptom of SAH
Sudden severe headache - worst headache of my life
May get brief LOC (raised ICP, ischaemia, seizure)
N/V, photophobia
Meningismus - neck pain/stiffness, positive kernigs sign
Usually no focal neurologic signs unless bleeding occurs into the brain and CSF at the same time but may get CN palsy, hemiparesis
Occular haemorrhage due to sudden raised ICP compressing central retinal vein
Reactive HTN
Differential diagnosis of severe sudden onset headache
SAH
Sentinel bleed
dissection/thrombosis of aneurysm
Venous sinue thrombosis
benign exertional headache
What is a sentinel bleed
SAH like symptoms lasting < 1 day (thunderclap HA)
May have blood on CT or LP
50% of patients with full blown SAH give history suggestive of sentinel blled within past 3 weeks
Risk factors for SAH
HTN
Pregnancy/parturition in patients with pre-existing AVMs, eclampsia
OCP
Substance abuse (smoking, cocaine)
Conditions associated with high incidence of aneurysms (e.g., polycystic kidney disease, fibromuscular dysplasia, connective tissue disease)
Investigations for suspected SAH?
FCB, coags
Non contrast CT - NB may be negative if small bleed or presentation delayed several days
CTA/MRA/cerebral angiography (gold standard) - localisation and treatment planning
If CT -ve do LP for xanthocrhomia (yellow appearance of CSF to indicate presence of RBCs)
LP opening pressure > 18mmH2O
What is cerebral perfusion pressure
MAP - ICP
MAP = DP + 1/3 (SBP-DBP)
Outline the immediate and early medical/surgical management of a patient with SAH
1. Coagulation problem
Coag screen if abnormal consider FFP and/or Vit K if PT or aPTT > 1.3; If warfarin or antiplatelet cease
2. DVT prophylaxis
- TED stockings - no heparin or clexane
3.BP
if S< 160 D < 100 - no BP lowering, monitor half hourly
if S > 160 D > 100 on 2 separate recordings 5 mins apart - clonidine or hydralazine
4. Neurosurgical management
if aneurysm - clip or coil - decreases risk of early and late recurrences
5. Stool softeners, bedrest, anaglesia
Complications with SAH
Vasospasm
hydrocephalus
neurogenic pulmonary oedema
hyponatraemia
DI
arrhythmias
What is vasospasm
constriction of blood vessels in response to arterial blood clot outside of vessels at the base of the brain
When is the usual onset of vasospasm?
4-14 days after SAH
Symptoms of vasospasm
LOC
focal deficit (speech or motor)
confusion
What is the triple therapy for vasospasm
Hypertension
Hypervolaemia
Haemodilution
Risk factors for vasospasm
smoking
increased age
prior HTN
large amount of blood on CT
Why do you get hydrocephalus with SAH
blood obstructs CSF drainage or subarachnoid space
What is the classic site of hypertensive haemorrhages
basal ganglia
you can also get them in the putamen, thalamus, cerebellum and pons
Clinical features of infarction of ACA
Primarily foot and leg involvement (motor and sensory)
Incontinence (loss of bladder control - hypertonic detrusor)
grasp reflex
Clinical features of middle cerebral artery
Hemiparesis and sensory (contralateral)
homonomyous hemianopia (optic radiation)
If dominant hemisphere - aphasia, Gerstmann syndrome in parietal (agraphia, acalculia, R/T finger agnosia)
Non-dominant - contralateral neglect, dressing and construction apraxia
Clinical features of infarction of lenticulostriate arteries
pure motor hemiparesis and hemisensory deficit
Ataxia +/- dysarthria
Clinical features of infarction of basilar artery
quadriplegia and death unless there are good anterior collaterals
generalised weakness, gait difficulty, decreased responsiveness progressing to coma. dysarthria, shivering, blurred vision
Clinical features of occlusion of PCA
homonymous hemianopia
Features of PICA infarction i.e. lateral medullary syndrome
ipsilateral ataxia
ipsilateral horners
ipsilateral facial sensory loss
contralateral impairment of pain and temp
nystagmus
vertigo
N?V
dysphagia and dysarthria
NO MOTOR HEMIPARESIS
What is the pattern of LP results for fungal infections and TB
increased protein
Decreased glucose
Increeased lymphocytes
which thumb mm does the median nerve supply?
opponens policis brevis
flexor pollicis brevis
What nerve supplies thumb adduction?
ulnar nerve
How does someone with a lacunar infarct present?
Basal ganglia, thalamus, posterior limb internal capsule
Pure motor hemiparesis: contralaeteral arm, leg, and face
Pure sensory loss: hemisensory loss (usually thalamic)
ataxix hemiparesis: ipsilateral ataxia and leg paresis
Dysarthria-clumsy hand syndrome (dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness)
Occlusion of which artery usually leads to locked in syndrome?
proximal basilar artery
Where is the lesion if you have loss of pain and temperature on the right side of the boyd and the left side of the face?
which artery is affected?
left medulla
lateral medulla or wallenburg syndrome
PICA
What is the hallmark sympom of vertebro basilar insufificneyc
vertigo
Cna also have nystagmus, limb ataxia, truncal ataxia, contralateral pain and temp,
CN - visual field defects
Hemi-or quadriplegia
Signs of upper motor neuron lesion
weakness
hyperreflexia
increased tone
up-going Babinksi

**refelxes and tonicity may develop over days/weeks and may look like LMN in the beginning
Signs of lower motor neuron lesion
weakness
atrophy
fasiculations
hyporeflexia
hypotonia
ABSENT Babinksi
Where is the lesion?... in one sided face, arm, leg weakness/paralysis WITHOUT sensory features
must be above medulla and below cortex

most common site = contralateral internal capsule

supplied by MCA/lentriculostriate system
What is a lacunar infarct?
Lacunar infarcts are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%). They occur less commonly in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum.

usually only motor is affected!
Where is the lesion?... in one sided face, arm, leg, weakness/paralysis WITH sensory, oculomotor, visual, higher cortical deficits
infarct of precentral motor strip w involvement of sensory neurons across the central sulcus

large territory MCA stroke, could be involving internal capsule
Where is the lesion...??

one sided arm and leg weakness/paralysis
face is spared - lesion must be below foramen magnum

two areas:
1. contralateral arm and leg regions of primary motor strip - more likely if acute

2. ipsilateral (below pyramidal decussation) corticospinal tract from caudal medula (after corticobulbal tracts have departed) and above C5 - more likely if gradual, could be neoplasm
if the face is spared, where must the lesion be in a TIA/stroke?
below the foramen magnum

because most of the CN efferents and the corticobulbar system remain largely above the foramen magnum
Where is a watershed infarct most likely?
between territories of anterior and middle cerebral arteries

gives rise to proximal mm weakness - man in a barrel syndrome
Where is the lesion...??

One-sided arm and face weakness/paralysis
precentral motor cortex (face and hands are side by side on the homonculus)

usually associated with Broca's aphasia if in dominant sphere, hemi-neglect in non-dominant

most common cause = MCA (superior division)
Where is the lesion..??

One-sided arm weakness/paralysis
can be:
1. peripheral nerve lesion - check for LMN signs... but would most likely have sensory signs too, CANNOT have pure motor loss unless lesion is just in anterior horn

2. discrete infarct affecting just contralateral are of precentral motor cortex - will have UMN signs
Where is the lesion...?

one sided leg weakness/paralysis
could be:
1. leg region of precentral motor cortex - infarct of anterior cerebral artery

2. CsT below T1 (bc no arm weakness) - compression by tumor or MS

3. peripheral nerves supplying leg - injury or diabetes, but would probably have sensory loss too
Where is the lesion...??

Unilateral facial weakness/paralysis
Bell's palsy - CNVII, usually 2ary to Herpes Zoster

could also be contralateral precentral motor strip, but would probably have arm and leg involvement

if UMN lesion --> forehead and eyes will be spared
Where is the lesion...??

Bilateral arm weakness/paralysis
bilateral medial portions of CsT aka central cord syndrome caused by syringomyelia or myelitis
Where is the lesion..??

Bilateral leg weakness/paralysis
could be:
1. parasagittal meningioma
2. bilateral infarct of anterior cerebral artery
3. CsT below T1 - may also present with cauda equina syndrome, which would involve sensory loss
4. neuromuscular disorders (GBS, lambert eaton, diabetic) - usually affects proximal mm
Where is the lesion...??

bilateral arm and leg weakness/paralysis
could be:
1. bilateral motor strip

2. CsT after leaving foramen magnum but before reaching C5

3. cord transection above C5 - would have UMN signs, sphincter dysfunction, autonomic dysfunction
What are the lab values in Duchenne's muscular dystrophy? (CK, nerve conduction, EMG)
CK: elevated, goes down in terminal stages of disease
nerve conduction: normal
EMG: grossly abnormal
Definitive diagnostic test in Duchenne's muscular dystrophy
immunohistochemical staining of mm biopsy --> absent dystrophin molecule
Rx of dermatomyositis and polymyositis
kids: almost always respond to steroids
adults: often require immunosuppressive therapy with azathioprine + corticosteroids
What is Wilson's disease and what is the Rx?
excessive copper deposition --> degeneration of liver and basal ganglia --> dystonia, dysarthria, rigidity, tremor, chorea, psych

serum copper high, ceruloplasmin low

Rx: copper-chelating agent (penicillamine)
Difference between Parkinsons's and multisystem atrophy
MSA is usually symmetrical, absence of resting tremor, and little response to dopaminergic agents
Rx of acute angle closure glaucoma
reduce IOP --> acetazolamide or laser peripheral iridotomy

also, alpha agonists, cholinergic agents (pilocarpine), beta blockers, prostaglandins
What is cabergoline and what are its SEs?
Dopamine receptor agonist

SEs: pulmonary, retroperitoneal, and cardiac fibrosis
(same for all dopamine receptor agonists! bromocriptine, ropinirole, apomorphine)
Signs of acute angle closure glaucoma
headache, painful and red eye, seeing halos, N&V, reduced VA
CSF values in bacterial and viral meningitis
Bacterial: cloudy, low glucose (<1/2 plasma), high protein, WCC 10-5000 polymorphs

Viral: clear/cloudy, normal glucose*, normal/raised protein, WCC 15-1000 lymphocytes

Mumps and herpes encephalitis can be associated with low glucose level
Are reflexes normal in polymyositis?
yes
Middle cerebral artery stroke symptoms
1. contralateral face-arm-trunk motor & sensory deficit

2. Broca's (superior branch) or Wernicke's (inferior) aphasia OR neglect if lesion in non dominant hemisphere

3. homonymous hemianopia

4. gaze preference toward side of lesion
Anterior cerebral artery stroke symptoms
1. contralateral hemiparesis and sensory loss in leg

2. frontal lobe dysfunction
Posterior cerebral artery stroke symptoms
1. homonymous hemianopia

2. if affects corpus callosum --> alexia
Lenticulostriate artery stroke symptoms
1. pure motor or sensory hemiparesis
2. ataxic clumsy hand +/- dysarthria
Does small vessel disease have a greater effect on whtie matter or grey?
white matter
More capillaries in grey matter - high metabolic demand - therefore if you interupt a few small vessels in grey matter won't get infarction - enough to ensure survival
How often does focal ischaemia in brain produce unconcsioussness?
very rarely
What is transient globlal amnesia?
unable to lay down new memories
migraine equivalent that produces spasm in basilar artery or in distal territory - iscahemia of mesotemporal lobe that disables both hippocampi
New goes onto stroke - a couple of hours where they can't lay down memories
Do you see neglect in dominant hemisphere strokes?
not very often
Only if it is a very large stroke
Otherwise usually just see neglect in non-dominant MCA strokes
What features will you have in a non dominant hemisphere MCA stroke? cf dominant?
contralateral neglect
navigational difficulty
dressing apraxia
constructional apraxia
Dominant
aphasia
Gerstmann syndrome, agraphia, acalculia, R/L confusion, finger agnosia
Do you get a visual field defect with ACA?
NO
Which artery supplies the macula?
distal MCA
If you get bilateral infarctions of PCA what do you present with?
bilateral hemianiopa with cortical blindess
associated memory disturbance
Emoblus lodges at top of basilar?
cortical blindness and often quadriparesis (damaged blood supply to cerebral peduncles - containing outflow from internal capsule)
Which group is basilar occulsion common in?
elderly
tortuous vessels
Often present with slow progression to coma
How do small vessel infarcts present?
Each is own syndrome - features may not occur toegether
pure hemiparesis - no sensory deficit or aphasia etc
ataxic clumsy hand
both of the above can occur in internal capsule and somewhere in pons
clumsy hand + dysarthria
pure hemi sensory deficit
what is the significance of transient hemiparesis?
medical emergency
signals impending stroke
What heralds the onset of an uncal herniation?
unialtaeral 3rd nerve palsy
contralateral weakness - compressing cerebrellar peduncles

Uncus is area of temporal lobe right near medulla
What causes apneustic respiration?
= prolonged pauses in respiration
caused by pontine lesion
What causes ataxic respiration
= irregular respiration
medullary lesion
poor prognosis
What can cause pin point pupils?
opiate overdose
pontine lesion
Which direction are the eyes deviated towards in a supratentorial lesion?
pontine lesion?
Supratentorial lesion - towards lesion - centre on that side has been destroyed, contralateral centre pushes eyes to side of lesion
Pontine lesion - away from lesion - horizontal gaze centre lateral aspect of pons - moves eyes to same side if destroyed moves eyes away
What is the oculocephalic reflex
moves head - eyes will stay fixed or move away from side that you're moving head to
decreased OC - eyes will move with head = dolls eye movement - eyes are not being moved as they should be by vestibular system
What is the oculovestibular reflex?
squirt hot and cold water into ear drum
cold water - eyes move to side of lesion
hot water - move away from side of lesion
Vestibular lesion - this is lost
Where is the lsion in decererbate rigidy?
midbrain lesion
Where is the lesion with decorticate posturing?
corticospinal damage
how long do brain reflexes need to be absent before you can pronounce brain death?
24 hours
Which tests can you do to determine brain death?
ALL must be absent for 24 hours
pupils fixed and dilated
caloric reflexes absent
corneal reflexes absent
no reflex to noxious stimuli
gag reflex absent
NO spontaneous respiration
patients must not be on any sedative agents
exclude reversible causes