Revision 2 Flashcards
what area is affected early in alzheimers
nucleus basalis of meynert (group of CHOLINERGIC neurones)
what is the treatments for alzheimers
acetylcholinesterase inhibitors- donzepezil, galantamine, rivastigime (monotherapies) for milf to mod
memantine (NMDA receptor antagonist) for severe/ AChEi CI
what mutation= 100% penetrance of huntingtons
40 or more CAG repeats
what types of inheritance does huntingtons have
genetic anticipation
autosomal dominant
what are parkinson plus syndromes
diseases that cause parkinsonism + other symptoms:
- multi system atrophy
- dementia with lewey bodies
- progressive supranuclear palsy
- corticobasal degeneration
what is multi system atrophy
group of disorders that progressively affect the central and autonomic nervous by system damaged oligodentrocytes (myelination) by accumulation of alpha synuclein
two types- MSA-P: characterised by parkinsons motor symptoms, deteriorates faster. MSA-C: cerebellar, lack of coordination and balance, intention tremor, slurred speech and difficulty swallowing (dysphasia)
both types characterised by autonomic symptoms- orthostatic hypotension, constipation, increased sweating, sleep apnoea, sexual dysfunction
what protein is found in dementia with lewey bodies
alpha synuclein
what are the symptoms of DLB
cognitive impairments, visual hallucinations, inability to focus, inflexible thinking and paranoia. DLB patients initially have these cognitive symptoms but also develop motor symptoms similar to PD such as bradykinesia, tremor, rigidity, and shuffling walk. Similar to PD, DLB patients also have REM sleep behavior disorder in which they act out their dreams.
what is progressive supranuclear palsy
chronic neurodegenerative syndrome which affects cognition, eye movements and posture
what are the symptoms of progressive supranuclear palsy
supranuclear (primarily vertical) gaze palsy
extrapyramidal - akinesia
cognitive dysfunction
postural instability
vague fatigue, HAs, arthralgia, dizziness, depression, modd changes, progressive dementia
what is a supranuclear palsy
the inability to look in a particular direction as a result of cerebral impairment:
- frontal lobe (frontal eye field)-> pontine horizontal gaze centre (PPRF) -> abducens nucleus-> lateral rectus
- occipital cortex-> oculomotor nucleus -> CN3 and medial longitudinal fasciulus -> pontine horizontal gaze centre
loss of voluntary movements of eye
as brainstem intact, all reflex conjugate eye movements normal
how do you distinguish a vertical gaze palsy from a cranial nerve palsy
both eyes affected
pupils unequal but fixed
no diplopia
reflexes intact
what is corticobasal degeneration
where multiple areas of the brain atrophy
begins around 60
start unilateral then go to other side
- poor coordination, rigidity, impaired balance, dysphagia
-personality changes, inappropriate behaviours, compulsive behaviours
what causes most postural tremors
essential- autosomal dominant inheritance, gets better when you drink alcohol
what is a treatment for an essential tremor
propanolol
what does an intention tremor suggest
cerebellar diseases
how does huntingtons usually present
strange movements and behavioural changes
what is sydenham chorea
form of chorea that is more common in females adolescents and linked to rheumatic fever (group A beta haemolytic strep infection)
what does myoclonus look like
brief electric shock like movements
e.g. 20 y/o guy gets milk but drops it= juveline myoclonic epilepsy
why is alzheimers linked to downs syndrome
alzheimers cause by beta amyloid precursor protein (insoluble, forms plaques which disrupt neuronal signalling) and the gene that codes for this is on chromosome 21 (trisomy 21= more production of amyloid= build up of plaques)
loss of dopaminergic neurones in the substantia nigra =?
parkinsons disease
what does the globus paladus alway inhibit
the thalamus - main job of direct pathway is to reduce this inhibition
what is the tremor like in parkinsons
resting
4-6 Hz
pill rolling
starts on one side then becomes bilateral
sudden onset bilateral parkisons with resting tremor= ?
drug induces parkinsonism
name two drugs that can cause drug induced parkinsons
dopamine antagonists: haloperidol, metoclopramide
what is hemiballism
wild movements of one arm/leg caused by an infarct of the subthalamic nucleus (part of the indirect pathway)
how is hemiballism treated
self limiting
treated over a few months with antipsychotics
parkinsonism with orthostatic hypotension and has a poor response to levodopa =?
multi system atrophy
where is the lesion in vascular parkinsons
infarcts in basal ganglia
how do the symptoms of vascular parkinsons differ from normal parkinsons
vascular is more prominent in the lower limbs, resting tremor in legs
what causes syndenhams
infection with group A beta haemolytic strep causes rheumatic fever- when infected antibodies from against basal ganglia and cause syndehams
clear CSF with normal opening pressure
oligoclonal bands present
MS
clear csf with normal opening pressure
lymphocytes present
high protein
normal glucose
viral
what are the signs of IIH
high CSF opening pressure bilateral papilloedema (can progress to blindness)
what is the management for IIH
1st line weight loss
2nd line acetalozamide
3rd line shunt
is there CSF in the subarachonoid space
yes
yellow tinge in CSF 12 hours after haemorrhage = what type of haemorrhage
SAH
can SAH be spontaneous or traumatic
both
is viral meningitis more/less intense than bacterial/ TB meningitis
less intense
what are all meningitis’ treated as until proven otherwise
bacterial
what is the Tx for viral meningitis
supportive
cloudy CSF elevated opening pressure neutrophils (aka polymorphs/ polymorph pleocytosis) present high protein low glucose
bacterial meningitis
opaque CSF if left to settle forms a fibrin web elevated opening pressure lymphocytes present high protein low glucose
TB meningitis
best initial test to diagnose:
alzheimers
MMSE
- will have impaired recall
- lose short term memory
- retain long term memory
- eventually become disorientated to time, place and person
best initial test to diagnose:
frontotemporal dementia
MRI
-will show focal atrophy in frontal and superior temporal lobes
what is picks disease
FTD
how will FTD present
behavioural symptoms, self neglect, language (lose vocab)
what is FTD associated with
MND
how is FTD different from huntingtons
not inherited
has no chorea
best initial test to diagnose:
-vascular dementia
MRI
-shows long term damage from infarcts
what is the classic presentation of vascular dementia
step wise cognitive deterioration - result of multiple infarcts
which anti-epileptic drug:
used in pregnancy
SEs: rash, SJS
lamotrigine
least teratogenic, given with folic acid
which anti-epileptic drug:
used for treatment of absence seizures, blocks the thalamic T type Ca2+ channels
ethosuximide
what are absence seizures
usually happen in children
go completely blank
wont move/ remember it then snap out of it
which anti-epileptic drug:
Na+ channel activation
increase GABA concentration
should be avoided in women of childbearing age
used for majority of generalised seizures
SE: weight gain, alopecia
is a P450 enzyme inhibitor
sodium valoprate
highly teratogenic
what is a simple partial seizure
mini electrical disturbance in part of the brain
will have awareness of what is happening
can be motor (frontal lobe), visual (occipital lobe), sensory (parietal)
what is a complex partial seizure
involves a bigger bit if the brain
may have aura- hear/ see feel something abnormal/ will have de ja ve (with itself can be seizure)
then loss of awareness
confusion/ drowsiness after seizure = the post ecter phase
(aura, loss of awareness, post ecter ohase)
what type of seizures is an absence seizure
generalised
what is the tonic phase of a seizure
stiffening of whole body, stiff, rolling eyes back
what is the clonic phase of seizure
jerky movements
what does loss of awarness in a seizure mean
it cannot be a simple partial
what is a generalised seizure
seizure type characterised by loss of consciousness, widespread motor manifestations of tonic contractions followed by clonic jerking movements, and a suppressed level of arousal following the event (post ecter phase)
May either reflect an underlying generalised-onset epilepsy or focal epilepsy that has secondarily generalised.
what are non epileptic seizures
not caused by abnormal electrical activity in brain
can be psychogenic
will not have post ecter phase
movement is not coordinated
what treatment for non generalised seizures
(simple and complex partial seizures)
carbamazepine
what is the first line Tx for absence seizures
sodium valporate/ ethosuximide
1st line for generalised tonic clonic seizure
sodium valporate
what is status epilepticus
seizure lasting more than 30 mins
what is the Tx for status epilepticus
at 5 mins give IV lorazepam
best long term management:
uncontrolled hypertensive who develops a stroke
antihypertensives
BP control
best long term management:
patient who has a seizure due to a CVA
carbamazepine
best long term management:
patient with an ischaemic stroke is found to have AF
warfarin
best long term management:
ischaemic stroke
(acute treatment is aspirin in first 2 weeks)
lifelong clopidogrel
most useful Ix to order:
65 y/o male patient presents to the clinic with double vision and ptosis
he has weakness that gets worse during the day
anti AChR (acetylchonine receptor) antibodies (diagnosis here is myasthenia gravis- antibodies against post synaptic channels, affects the eyes)
what are the features of lambert eaton syndrome
auto immune condition against pre synaptic channels
weakness of limb muscles
associated with small cell lung cancer
what antibodies for lambert eaton
anti musk
which medication:
20 y/o female with tonic clonic seizures which wants to conceive soon
lamotrigine
which medication:
patient with epilepsy on medication presents with these SEs- blurred vision, vertigo and blood results reveal a hyponatremia
carbamazepine
which medication:
a mother has noticed her 8 y/o daughter has been day dreaming and not paying attention
after discussing with GP an EEG was organised which revealed a 3Hz spike wave
ethosuxomide
best management:
58 year pld man with ischaemic heart disease requires treatment for an acute migraine attack that has not responded to paracetamol
high dose NSAIDs with antiemetic
best management:
25 year old male who presents with right sided supraorbital pain and ipsilateral ptosis and miosis
pain lasts 30 mins and usually occurs at same time every night
high flow oxygen with SC sumatriptan
(diagnosis is a cluster HA)
long term management for cluster HAs is verapamil
what are the features of a cluster HA
Stabbing pain around orbit or in temporal lobe. Have circadian rhythm, last 30 mins to 3 hours.
how long do migraines last
5-72 hours if untreated
what part of head to migraines affect
are hemicranial
best management:
55 year old female patient presents with left sided supraorbital pain with ipsilateral nasal congestion. This occurs about 20 times a day and lasts about 10 minutes
indomethacin
diagnosis is paroxysmal hemicrania
how is paroxysmal hemicrania different from cluster HAs
occurs more frequently
lasts shorter amount of time
how do you control vomiting in a patient with parkinsons
domperidone (is a dopamine antagonist but doesnt cross BBB)
what medication:
Patient on therapy for parkinsons develops acute psychosis
quetiapine
pick secondary generation antipsychotics as first gen will worsen parkinsons
what medication:
dyskinesia is a SE of this drug used in the treatment of parkinsons
levodopa
acts as dopamine for the brain but over time can cause excessive unwanted movement (dyskensia)
how is dyskensia prevented when levodopa is given
not given on its own, given with dopadecarboxylase inhibitor which prevents peripheral conversion of the drug to dopamine
what medication:
1st line for parkinsons
levodopa
causative organism:
pregnant lady presents with signs of meningism
culture reveals gram +ve flagellate rods
listeria
tends to affect young babies, elderly and pregnancy women
how is listeria meningitis treated
amoxicillin
Causative organism:
18 y/o uni student presents with stiff neck, photophobia and fever
cultures reveal a gram -ve diplococcus
neisseria meningitidis
what is the excitatory neurotransmitter
glutamate
what is the inhibitory neurotransmitter
gaba/glycine
name two opioid antagonists
naloxone and naltrexone
what are alpha and delta nerve fibres
mechanical/ thermal nociceptors that are thinly myelinated (first response- sharp pain)
what are C fibres
unmyelinated
are second response- throbbing pain
what is the role of astrocytes
maintain BBB
what is the role of oligodendrocytes
myelination of CNS
what is the role of schwann cells
myelination of PNS
what is the role of ependymal cells
CSF regulation
what is the role of microglia
phagocytes
what is the role of the inf and sup articular processes on vertebrae
mobilise with adjacent vertebrae via synovial facet joints
where on a vertebrae does the rib articulate
transverse processes
where do the anterior and posterior rami supply
anterior- anterolateral body wall
posterior- posterior body wall
is the anterior or posterior rami bigger
anterior
which part of the grey matter butterfly gives of anterior roots
top wings
name the ascending tracts
dorsal column- fasiculus gracilis and cuneatus
dorsal and ventral spinocerebellar tract
fasciculus proprius
spinothalamic and spinoreticular tract
name the descending tracts
medial longitudinal fasciculus lissauers tract lateral and ventral corticospinal tracts rubrospinal tract pontine reticulospinal tract meduallry reticulospinal tract lateral vestibulospinal tract tectospinal tract
summaries the DCML
fine touch
conscious proprioception
fibres cross in the medulla
summarise the spinothalamic tract
pain, temperature, deep pressure
fibres cross segmentally
summarise the corticospinal tract
fine precise movement, particularly of distal limb muscles
forms on the medulla - pyramidal tract
85% of fibres cross in the caudal medulla at the decussation of the pyramids
where is the primary somatosensory cortex
post central gyrus in the temporal lobe
where is the primary motor cortex
pre central gyrus, frontal lobe
where is the lesion in decoricate posturing
(flexor)
cervical spinal tract/ cerebral hemisphere
rubrospinal tract dominant
(decorate things red at christmas)
where is the lesion in decerebrate posturing
(extensor)
midbrain/ pons
vestibulospinal tract prominant
from medial to laterla in the primary motor cortex, list the parts of body controlled by each bit of brain
foot hip trunk arm hand face tongue larynx
what is the role of the basal ganglia
modulates motor control
what makes up the basal gamglia
caudate putamen globus pallidus subthalamic nucleus substantia nigra
what are the functions of the frontal lobe
voluntary movement reasoning executive function personality inhibition initiative expressive language habit learning emotional control
what are the functions of the parietal lobe
knowing left from right reading writing body orientation calculation two point discrimination graphaethesia
what do lesions in the DOMINANT parietal lesion cause
dysphasia
dyscalculia
dyslexia (difficuly learning to read. interpret words, letters and symbols)
apraxia
agnosia
gerstmann syndrome (acalculia, agraphia, finger anomia, difficulty in differentiation of right and left)
what is apraxia
inability to perform complex movements in the presence of normal motor, sensory and cerebellar function
what is agnosia
tactile- inability to recognise or discriminate objects through touch
what is agraphia
inability to write
what is finger anomia
cant recognise own or other peoples fingers
what does a lesion in the NON DOMINANT parietal lobe cause
spatial disorientation
constructional apraxia
dressing apraxia
anosognosia (lack of self awareness of own medical illness)
what are the functions of the temporal lobe
understanding speech memory hearing emotions sense of identity recognising faces
what do strokes in the dominant half of brain often have
language affected which has major implications for rehab
what is the acute treatment for an ischaemic stroke
Alteplase clot buster 0.9 mg/kg (max 90mg)
10% over 60 mins
Rest over 8 hours
MUST be given within 4.5 hours of symptom onset
what is a TACS
total anterior circulation stroke
all three of:
-unilateral weakness and/or sensory weakness of face, arm and leg
-homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)
what is a PACS
partial anterior circulation syndrome
two of:
-unilateral weakness and/or sensory weakness of face, arm and leg
-homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)
what is a POCS
posterior circulation syndrome one of: -cerebellar/ brainstem syndrome -loss of consciousness -isolated homonymous hemianopia
what is a LACS
lacunar syndrome (subcortical stroke due to small vessel disease)
one of:
-unilateral weakness and/or sensory deficit of face and arm, arm and leg or all three
-pure sensory stroke
-ataxic hemiparesis
what do subdural haematomas look like on MRI
banana
explain the slow onset of symptoms in a subepidural haematoma
bridging veins rupture
these are low pressure so blood spreads around brain before displacing it, gradual increase in symptoms
what vessel is classically ruptured in an extradural haemorrhage
middle meningeal artery (runs under pterion)
what is the formula for cerebral perfusion pressure
CPP= MAP - ICP
how do you remember how much each segment of the GCS scores
eyes (four letters)
speak (five letters)
motor (M6 motorway)
what is the minimum GSC score
3
what GCS score= coma
<8
what are the headache red flags
new onset headache >55 known/ previous malignancy immunosuppressed early morning HA excerbation by valsalva significant trauma in Hx coagulopathy with trauma
what is the management for migraines
Diary to find triggers – then exclude triggers
NSAIDS eg 900mg Aspirin
Triptans (oral first) - must be at start of headache and repeated only once.
More than 3 attacks in a month – prophylaxis:
-Propranolol
-Topiramate (loads of side effects, start slow)
Remember contraception issues in women
what are the symptoms of trigeminal neuralgia
severe stabbing unilateral pain, v severe
Duration: 1sec to 90 secs
Frequency: 10 to 100 day
Bouts pain may last from a few weeks to months before remission
more common in females
any frequency
cutaneous trigger
what is the main drug used to treat trigeminal neuralgia
P450 inducer
what can trigger cluster HAs
alcohol
what are the features of a cluster HA
more common in males boring pain V. severe orbital 15-180 mins 1-8 per day autonmic features
what are the features of paroxsymal hemicrania
more common in females boring pain v severe orbital lasts 2-45 mins 1-40 per day autonomic features responds to endomethicin mechanical trigger
what are the features of SUNCT
(short lasting unilateral neuralgiform HA with conjunctival injection and tearing) more common in women stabbing pain severe orbital 15-120 seconds 1 a day- every 30 hours autonomic features cutaneous trigger
what are the features of a stabbing/ icepick headache
more common in females stabbing pain severe anywhere in head lasts <30 secs any prequency autonomic features no trigger responds to indomethicin
summarise brown sequard syndrome
hemicord lesion
- lateral corticospinal tract damage = ipsilateral UMN weakness
- posterior column= ipsilateral vibration and proprioception loss
- anterolateral system= contralateral pain and temperature loss
describe the symptoms seen in central cord syndrome
centre part of spinal cord affected
in small lesions- spinothalamic tract fibres that cross the anterior white matter commisure are interrupted = bilateral pain and temp loss at affected levels, below this cord function intact = cape like distribution
large lesions- corticospinal, spinothalamic and dorsal column may be affected aswell= upper motor neurone pattern of deficit below the level of injury (interrupted corticospinal), with spastic paralysis and urinary retention, and a LMN deficit pattern at level of injury (damage to ant horn cells)
upper extremities more affected than lower as fibres more central
which nerve is at risk of injury:
colles fracture
median
which nerve is at risk of injury:
ant shoulder dislocation
axillary
which nerve is at risk of injury:
humeral shaft #
radial (in spiral groove)
which nerve is at risk of injury:
posterior dislocations of hip
sciatic
which nerve is at risk of injury:
supracondylar # of the elbow
median (anterior interosseous branch)
which nerve is at risk of injury:
bumper injury to the lateral knee
peroneal nerve (fibular)
what differentiates back ache from sciatica
back ache can radiate to buttock and thigh but not below the knee like sciatica can
what are the symptoms of an L3/4 prolapse
> L4 root entrapment > pain down to medial ankle (L4), loss of quadriceps power, reduced knee jerk
what are the symptoms of an L4/5 prolapse
L5 root entrapment > pain down dorsum of foot, reduced power Extensor Hallucis Longus and tibialis anterior
what are the symptoms of an L5/S1 prolapse
S1 root entrapment > pain to sole of foot, reduced power planarflexion, reduced ankle jerks
what is the role of broca and wernickes areas
brocas- speech production
wernickes- speech comprehension
what are the SEs of sodium valporate
increased appetite= massive weight gain alopecia teratogenic (neural tube defects, cleft lip and palate, cardiovascular abnormalities, genitourinary defects, developmental delay, endocrinological disorders, limb defects, and autism)
what is lamotrigine first line for
focal seizures (carbamazepine is 2nd line) women with generalised seizures
what are the SEs of lamotrigine
rash
HA
dry mouth
what is levetiracetam
epilepsy management
2nd line in women of childbearing age
Good 3rd line alternative after sodium valproate and lamotrigine
Quite well tolerated – tiredness apathy weight gain
what are the key symptoms of MS
Optic neuritis, Sensory symptoms, Lr urinary tract dysfunction, Pyramidal dysfunction (Tone+, spastcicity, F of UL, E of LL)
At least 2 episodes suggestive of demyelination + Dissemination in time and place
what will be seen on blood tests for MS
nothing
what for acute Tx for MS flare
steroids
what are the treatment options for parkinsons
levodopa (with dopadecarboxylase inhibitor)
monoamine oxidase B inhibitor
dopamine agonist
can add on
catechol-o-methyl transferase inhibitor (prolongs actions of levodopa)
what are the symptoms of parkinsons
Gait - shuffling, slow turning with multiple steps, trouble with doorways, stooped over, reduced arm swinging, fenestration
Also non-motor features: EARLY - Hyposmia (reduced smell),
Constipation,
REM sleep disturbance (can act out dreams)
depression – V V common and pronounced generally
LATE - Dementia (it is Lewy body dementia if within the first 2 years, otherwise is parkinsons disease dementia)
Everyone gets some form of cognitive decline over time with parkinsons disease.
cog wheel rigidity
resting tremour)
positive froment’s maneuver (rigidity increases in examined body segment by voluntary movement of other parts),
micrographia,
bradykinesia,
hypomimia (decreased facial expression),
hypophonia (quieter voice)
which generation of antipsychotic is clozapine
2nd - is an atypical
name extrapyramidal drugs
(dopamine antagonists)
all antipsychotics- typicals (haloperidol) worse than atypicals (clozapine)
metoclopramide
domperidone
what is the main down fall of atypical antipsychotics
weight gain and metabolic syndrome
what causes meningitis in neonates
listeria, group B streptococci, E. coli
what causes meningitis in children
H influenza
what causes meningitis in ages 10-21
meningococcal
what causes meningitis in >21s
pneumococcal > meningococcal
what causes meningitis in the elderly
pneumococcal > listeria
what causes meningitis in immunocompromised
S. pneumoniae, N. meningitidis, Listeria, aerobic GNR (including Ps.aeruginosa)
what causes meningitis in patients who have had neurosurgery/ open head trauma
staphylococcus, gram -ve rods
S. aureus, S. epidermidis, aerobic GNR
what causes meningitis in patients with a # of the cribiform plate
pneumococcal
S. pneumoniae, H. influenzae, beta-hemolytic strep group A
what causes meningitis in patients who have a CSF shunt
S. epidermidis, S. aureus, aerobic GNR, Propionibacterium acnes
what is the management for meningitis
Ceftriaxone I.V 1.2mg bd +/- amoxicillin if over 60 (listeria cover)
Penicillin allergy:
Chloramphenicol + Vancomycin +/- co-trimoxazole (listeria cover)
If it is meningococcal - additional steroids are not required but everyone gets it until its established
what is the treatment for status epilectus
1st stage (0−10 minutes):
- Secure airway and resuscitate
- Administer oxygen
- Assess cardiorespiratory function
- Establish intravenous access – get help to hold site still
- Glucose (50 ml of 50% solution) and/or intravenous thiamine if appropriate
Pre-hospital - Diazepam 10−20 mg per rectum
1mg Midazolam buccally
In hospital - Lorazepam IV 0.1mg/kg with 4mg bolus (don’t worry about dose)
if unable to get IV access, go to rectal diazepam
This stage call MUST call senior/ICU
Established (20mins or more despite therapy) – IV phenytoin or fosphenytoin
MUST CALL ICU!!!
what is the mnemonic for things that can cause cerebellar symptoms
DAISIES Demyelination Alcohol Infarction SOL- schwannoma Inherited (wilsons, fredricks ataxia) Epilepsy medication (multiple) System atrophy
what is rhombergs testing
proprioception and sensory ataxia
wont be able to stay balanced with eyes shut
what type of nystagmus in cerebellar disease
horizontal
what is speech like in cerebellar disease
slurred staccato
what is the fast phase of nystagmus going towards
the side of the lesion
what happens to the tremor in parkinsons when counting back from 100
gets worse- gets worse on concentration
what type of tremor might a dopamine agonist cause
bilateral
can patients with parkinsons draw a neat circle
yes- have RESTING tremor
what does a babinski +ve test mean
claw out
UMN lesion
what is a bovine cough seen in
vagus nerve lesions
what disease are tongue fasciculations seen in
MND
