neuro (264) Flashcards
Ax Duchenne muscular dystrophy?
S/s
X-linked recessive - mutation in dystrophin gene results in dystrophin deficiency
s/s
* delay in motor development
* onset of weakness in 3-4 years
(Gower’s sign, toe walking, exaggerated lumbar lardosis, calf hypertrophy)
Dx DMD?
raised CK
genetic testing (dystrophin gene)
EMG
muscle biopsy
is DMD inherited?
2/3rds inherited from asymptomatic mother 1/3rd sporadic
huntington’s disease onset?
S/s?
Ax?
30-50 years
S/s
* dementia
* chorea
Ax = autosomal dominant CAG42
appearance of Huntington brain
flattening of normal convex curve of lateral ventricles - due to loss of ganglia from caudate nucleus

Spinal muscular atrophy Ax?
S/s?
Tx?
autosomal recessive - loss of anterior horn cells
* floppy/weak arms and legs
* breathing difficulties
Tx = synthetic oligonucleotide
Alzheimers brain appearance genes?
neurofibrillary tangles + amyloid plaques
AD (presenilin) in 5% of cases - usually multifactorial
ApoE4?
carriers more likely to get Alzhiemer’s in old age
classification meningitis
acute pyogenic (bacterial)
acute aseptic e.g. viral
chronic bacterial - TB
acute encephalitis
pyogenic meningitis dx?
suppurative exudate
neutrophils in subarachnoid space
Ax bacterial meningitis?
strep pneumo (gram +ve cocci)
neisseria meningitidis (gram -ve diplococci)
listeria (gram +ve bacilli) - seen in alcoholics, immunosuppressed, elderly or neonates
Tx bacterial meningitis
ceftriaxone! + dexamethasone
*if penicillin allergic = chloramphenicol
if at risk for listeria (alcohol, old, immunosuppressed) add amoxicillin
(ceftrizone does not cover listeria)
viral meningitis Ax?
Dx?
Tx?
enteroviruses e.g. ECHO virus
Dx = viral stool culture, throat swab, CSF PCR
Tx = supportive, self-limiting
encephalitis vs meningitis
s/s?
encephalitis = brain parenchyma
meningitis = meninges
encephalitis = confusion, behaviour disturbances, psychosis, altered consciousness, seizures
meningitis = fever, photophobia, headache, neck stiffness, ?rash
meningo-encephalitis = combo
Ax encephalitis
Ix
Tx?
Ax = herpes simplex
Ix = LP, EEG (abnormalities), MRI (temporal lobe)
Tx = IV aciclovir

Ax brain asbcess?
Tx?
strep + bacteroides
Tx = ceftriaxone
* if penicillin allergic = vancomycin
most likely cause of meningitis in
1 - neonates
2 - children
3 - ages 10-64
4 - over 65
5 - decreased immunity
6 - fracture of cribiform plate
7 - head trauma
neonates = listeria
children = haemophilus
10-64 = strep penumo
>65 = strep pneumo + listeria
decreased immunity = listeria
fracture of cribiform plate = strep pneumo
head trauma = staph
complications meningitis?
exudate around CN III + VI
brain abscess
cerebral oedema
communicting hydrocephalus
sources of infection meningitis
nasopharyngeal colonisation (sinusitis, otitis media)
remote foci of infection - endocarditis, pneumonia, UTI
when should lumbar puncture be avoided?
increased ICP
GCS <12
bacterial vs viral CSF

PCR meningitis?
used for viruses
are you more likely to see neisseria or haemophilus as cause of meningitis in children?
neisseria meningitidis because Hib vaccine?
most common cause of meningitis?
strep pneumo
tuberculous meningitis Tx?
isoniazid + rifampacin key
(pyrazinamide + ethamutol too)
Ax aseptic meningitis
Viral
malignancy
sarcoidosis
vasculitis
dural venous sinus thrombosis
drugs - co-trimox, NSAIDs
Tx listeria?
if penicillin allergic?
amoxicillin
if penicillin allergic = co-trimoxazole
contact prophylaxis meningitis?
500mg ciprofloxacin
vaccines meningitis?
neisseria - ACYW
Haemophilus - Hib
strep pneumo
glial cells CNS?
astrocytes - BBB
oligodendrocytes - myelin
epdenymal cells - ventricles
microglia - macrophages
red neuron?
hallmark of acute neuronal injury due to hypoxia e.g. stroke

example of inclusions?
neurofibrillary tangles in Alzheimer’s
oligodendrocite damage is a feature of?
demyelinating disorders
Gliosis?
astrocytes - scarring
most important indicator of CNS injury

types of microglia
M1 = acute
M2 = chronic
why does hypxoxia afect brain so much?
needs 20% total body oxygen
can only increse bloodflow 2-fold in response to hypoxia
excitotoxcity?
makes ischaemia worse
when can autoregulary brain mechanisms not compensate for BP?
when MAP falls below 50 mmHg
where in the brain are thromboembolic events most common?
middle cerebral artery
which areas of the brain are particularly sensitive to ischaemia?
watershed areas - zone between 2 arterial territories i.e. parieto-occipital
stroke?
sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
cerebral infarction Ax
thrombotic
* atherosclerosis - most common MCA!!
embolic
* from atherom ain internal carotid artery/aortic arch
rarer
* osteophytes compressing vertebral arteries
* vasculitis
* septal defects - right to left shunts
risk factors stroke
atheroma
hypertension
cholesterol
obesity
diabetes
drugs
smoking
septal defects
stroke after 12 hours
48 hours
a week
few weeks
12 hours = red neuron
48 hours = lots of micoglia
a week = gliosis begins
few weeks = gliotic scar
symptoms carotid artery infarct?
contra-lateral weakness or sensory loss
sometimes aphasia/apraxia
sudden severe headache
sudden vision loss
symptoms middle cerebral artery infarct?
weakness of contralateral face and arm
anterior cerebral artery infarct?
weakness and sensory loss in contralateral leg
vertebro-basilar artery infarct?
vertigo
ataxia
dysarthria
dysphasia
complex brain stem syndromes
lacunar infarcts Ax?
Affect?
multiple lacunar infarcts?
atherosclerosis/thrombus or distal embolism
affect basal ganglia
multiple = multi-infarct dementia
hypertensive encephalopathy symptoms?
signs?
symptoms
* severely hypertensive
* symptoms of raised ICP - headache, vomiting, altered balance, fits
signs
* global cerebral oedema
* tentorial and tonsillar herniation
* petechiae
types of intracrnaial haemorrhage
extradural haematoma = does not cross suture line
subdural haematoma = crosses suture line
subarachnoid hemorrhage
intracerebral haemorrhage

Ax intracerebral haemorrhage
causes of vascular injury - hypertension, amyloid angiopathy, diabetes, drugs (cocaine, alcohol), vasculitis
aneurysms
vascular malformations
coagulation disorders/iatrogenic anticoagulation
neoplasms
amyloid angiopathy Ax?
complication?
most commobly due to Alzheimers
complication = intracereberal haemorrhage (amyloid deposited in vessels causes rupture)
examples of vascular malformations in the brain
complications?
which are most likely to cause these complications?
arteriovenous malformations
cavernous angiomas
venous angiomas
capillary telangectases
can cause intracerebral haemorrhage, headaches, seizures + focal neurological deficits
arteriovenous and cavernous angiomas are most likely to cause intracrnaial haemorrhage
most common vascular abnormality?
where are they found?
arteriovenous malformation
MCA
subarachnoid haemorrhage Ax?
areas effected?
associated with?
most common cause is rupture of berry aneurysm
90% in territory of carotid artery
associated with ADPKD
subarachnoid haemorrhage risk factors
S/s?
common complication?
smoking, hypertension, drugs
s/s
* severe thunderclap headache
* vomiting
* loss of consciousness
complication = hydrocephalus
what seperates the 2 hemispheres?
what covers cerebellum
falx cerebri seperates 2 hemispheres
tentorium cerebelli covers cerebellum
normal CSF cytology
clear fluid
tiny amounts of lymphocytes
no neutrophils
no RBCs
no protein
glucose >2.2
will see neutrophils in bacterial meningitis
lymphocytes in viral meningitis
RBCs in SAH
hydrocephalus Ax
obstruction to CSF - inflammation, pus, tumours
decreased reabsorption of CSF - SAH, meningitis
overproduction of CSF - tumours of choroid plexus (very rare)
hydrocephalus classification
non-communicating = obstruction to flow of CSF within ventricular system
communicating = obstruction to flow of CSF outside ventricular system e.g. subarachnoid space or arachnoid granulations
timing of hydrocephalus

hydrocephalus ex vacuo
dilation of ventricular system + increase in CSF volume secondary to loss of brain parenchyma - Alzheimer’s disease
Ax raised ICP
increased CSF (hydrocephalus)
SOL
oedema
increased venous volume
physiological (hypoxia, hypercapnia, pain)
consequences raised ICP
intracranial shifts + herniations (e.g coning)
midline shift
pressure on cranial nerves
impaired cerebral blood flow
examples of herniations
tonsillar through foramen magnum

signs of raised ICP
papilloedema
headache
nausea + vomiting
neck stiffness
reduced consciousness
examples of SOLs
tumours
abscesses
haematomas
localised brain swelling i.e. oedema around infarct
symptoms + signs brain tumour
symptoms = heaahce (worse in morning), vomiting, seizures, visual disturbances
signs = focal deficit, papilloedema
brain tumours children?
adults?
children = below tentorium cerebelli
adults = above tenorium cerebelli
brain metastases
from?
far more common than primary brain tumours
* breast
* bronchus
* kidney
* thyroid
* colon
* melanoma
commonest primary brain tumour in adults?
children?
adults = astrocytoma
children = medulloblastoma
astrocytoma grading
grade 1 = pilocytic
* childhood, benign
grade 2 = well differntiated, some nuclear atypia but overall low grade appearance
grade 3 = more atypia
grade 4 = glioblastoma
* extreme atypia, necrosis
* 10-12 month survival
medulloblastoma?
found?
complication
Tx
most common tumour in children followed by pilocytic astrocytoma
occur in midline of cerebellum i.e. below tentorium cerebelli
complication = hydrocephalus
Tx = surgery + radiotherapy
brain abscess Ax
single abscesses = mastoiditis, chronic otitis media, sinusitis, dental infections, skull fracture (tend to occur adjacent to source)
multiple abscesses = haematogenous spread from bronchopneumonia, bacterial endocarditis, bronchiectasis, lung abscesses, congenital heart disease, IV drug use (tend to coccur at grey and white matter boundary)
appearance brain abscesses
S/s?
Dx?
Tx?
central necrosis, oedema, fibrous capsule
S/s = fever, raised ICP
Dx = CT, MRI (ring enhancing)
Tx = aspiration + antibiotics
brain abscess organisms?
strep, bacteriodes, staph
immunocompromised patients = fungi, toxoplasma in AIDS
why do contra-coup injuries tend to be worse despite being non-impact side?
denser CSF moves to coup side first
most common intracranial haematoma?
epidural
“burst lobe”
subdural + intracerebral haematoma
occurs mostly in frontal + temporal lobe
Ax epidural haematoma?
fracture of tempero-parietal region = midle meningeal artery
subdural haemorrhage Ax
disruption of bridging veins
(blood accumulates between dura and arachnoid mater)
acute vs chronic subdural haemorrhage
acute = elderly, cleat history of trauma
chronic = commin in injury but often no clear history of trauma

B - juvenile myoclonic epilepsy is generalised epilepsy so not associated with hippocampal sclerosis (focal)
important features in epilepsy history
onset - what were they doing? what did they look like? aura?
type of movements - rigor? clonus? tonic phase?
speed of recovery
ask about birth + development, family history, previous seizures (e.g. febrile fits), drugs, alcohol
social history - driving, occupation
what drug can make epilepsy worse
tramadol
Ix for epilepsy?
MUST DO ECG - prolonged Qt syndrome (most common presentation is episode of collapse)
CT to screen for injury
EEG
differential diagnoses epilepsy?
syncope
pseudoseizures, psychogenic
panic attacks
TIA
migraine
hypoglycaemia
parasomnia
paroxysmal movement disorders
cataplexy
tonic spasms of MS
driving rules epilepsy
1st seizure = 6 months (car), 5 years (HGV)
epilepsy = 1 year or 3 years during sleep (car), 10 years off medication (HGV)
types of epilepsy?
further classification?
focal + generalised (cortical network)
focal
* simple = without impaired consciousness
* complex = with impaired consciousness
generalised
* absence - petit mal
* myoclonic
* atonic
* tonic
* tonic clonic - grand mal
focal seizure locations + symptoms
Motor (frontal lobe) = rhythmic jerking, posturing, head and eye deviation, other movements (e.g. cycling), automatisms (e.g. plucking), vocalisation
(most common = movements of hands and face)
Sensory (parietal lobe) = omatosensory, olfactory, gustatory, visual, auditory
Psychic = memories, deja vu, jamais vu, depersonalisation, aphasia, complex visual hallucinations
generalised epilepsy onset?
tx?
e.g.?
onset = childhood + teens
Tx = sodium valproate
e.g. juvenile myoclonic epilepsy
* early monring jerks
* generalised seizures
* risk factors - sleep deprivation, flashing lights
focal epilepsy onset?
Ax?
Tx?
any age
Ax = underlying structural cause e.g. hippocampal sclerosis
Tx = carbamazepine
how to AEDs work?
activate GABA system
side effects sodium valproate?
weight gain, hair loss, fatigue
teratogenic!!
what drug is avoided in primary generalised epilepsy?
carbamazepine - can make way worse!
which AEDs induce hepatic enzymes?
carbamazepine, phenobarbital + phenytoin
(so avoid in POP and COCP)
status epilepticus?
Ax?
medical emergency - seizure activity >30 mins
Ax = hyponatraemia, pyridoxine (B6) deficiency, infection, head trauma, SAH, abrupt withdrawal of anticonvulsants, treating absence seizures with carbamazepine
convulsive status?
Complications?
Tx?
most dangerous form of status epilepticus - generalised tonic clonic fits without cessation
comps = hypoxia, hypotension, hyperthermia, rhabdomyolysis
Tx = ABCDE
* identify cause - infection, SAH, etc - so FBC, CT
* phenytoin + benzodiazepines!!
Tx epileptic seziure
IV lorazepam (1st line)
once stabilised = restablish normal AED Tx
if seizures don’t stop = IV phenytoin/phenobarbital
if still don’t stop = transfer to ICU for general anaesthesia
patient presenting with acute confusional state?
always suspect partial status epilepticus in addition to septic encephalitis (as they are difficult to distinguish)
functional attacks?
Ax?
Dx?
not epilepsy but patient has no control of attacks
related to trauamatic events, physical/sexual abuse, other stress, anxiety/depression
Dx = EEG + history
types of aura
Somatosensory auras = numbness, tingling, electric shocks, thermal sensations, pain
Visual auras = simple shapes, static, flashing, moving lights, colours
Auditory auras
Vertiginous auras = temporal-parietal lobe
Autonomic auras = temporal lobe (insula, amygdala, etc)
Tx functional attacks?
removal of epiletpic drugs
CBT
Tx of anxiety or depression
motor neurone disease?
s/s?
Untreatable and rapidly progressive neurodegenerative condition
s/s = muscle weakness, problems with speech, swallow problems, breathing problems
upper/lower motor neuron signs WITHOUT sensory problems
most common subtype MND?
ALS
prognosis MND?
average survival time = 3 years
Ax MND?
Types?
features of these types?
90% sporadic, 10% familial
types = ALS, PLS, progressive musclar atrophy, progressive bulbar palsy

ALS with fronto-temporal dementia associated with?
c9orf72 gene
upper vs lower motor signs in MND?

ALS symptoms?
PLS symptoms?
PBP symptoms?
ALS = mixed UMN and LMN signs
PLS = pure UMN
PBP (LMN) = wasting of the tongue, dysphagia, difficulty speaking (slurring)
progressive bulbar palsy will eventually become?
ALS

split hand syndrome?
ALS

C9orf72 mutation?
ALS with FTD
which subtype of MND has best prognosis?
primary lateral sclerosis
Ix MND?
EMG
neurological exam
Tx MND?
riluzole - gives an extra 3 months
communication needs
nutritional needs (dietician, gastrostomy) - metabolic rate in MND is doubled so weight loss expected
respiratory needs
sialorrhoea tx MND?
muscle cramps?
muscle spasms?
sialorrhoea = hyoscine/buscopan, glycopyronium (esp in cognitive impairment), botox
muscle cramps = quinine, baclofen
muscle spasms = baclofen, gabapentin
SOB MND?
lorezepam
S/s MND?
UMN/LMN signs without sensory issues
emotional lability i.e. inappropriate crying/laughing (early UMN sign)
cognitive impairment (50%) - ALS associated with FTD
* apathy, disinhibition, poor planning/decision making
hypokinetic vs hyperkinetic movement disorder
hypokinetic (too little movement) = parkinsons
hyperkinetic (too much movement) = tremor, tics, chorea, myoclonus, dystonia, athetosis
important points in history for movement disorders?
birth history - anoxia, perinatal problems, milestones
family history
drug and toxin history - neuroleptics, antiepileptics, illicit substances, toxins
s/s parkinsonism/akinetic rigid syndrome?
TRAP
tremor
rigidity
akinesia/bradykineasia
postural disturbances (flexed posture, postural instability)
how to distinguish rigidity from spasticity?
rigidity = no increase with higher mobilising speed
spacticity = yes!
positive froment’s maneuver?
parkinson’s (rigidity increases in examine dbody segment by movement of other body parts)
not to be confused with froment’s test for ulnar nerve palsy (adductor pollicis)
camptocornia?
extreme anterior truncal flexion sometimes seen in Parkinson’s
parkinsonian gait?
slow shuffling steps
decreased arm swing
slow turning with multiple small steps
festination
postural instability (pull test)
types of tremor?
resting - occurs when body part at rest
postural - occurs when arms outstretched
kinetic - occurs during movement of body part
dystonia?
Ax?
sustained intermittent muscle contractions
chorea?
Ax?
irregular purposeless movement
can be difficult to distinguish chorea from myoclonus (chorea shifts from one body part to another)
Ax = drugs (COCP), basal ganglia lesions, Sydenham’s chorea (rheumatic fever), APS, Huntington’s, neuroacanthyocytosis
Myoclonus
electric shock like jerks
caused by brief activation of a group of muscles leading to jerk of affected body part
ballism?
suggestive of?
severe type of chorea
involves proximal joints resulting in large movements
strongly suggestive of contralateral lesion involving striatum of subthalamic nucleus
essential tremor?
seen when?
what makes better?
most common type of postural tremor (not associated with Parkinson’s = resting tremor)
seen in hands (5Hz) while holding outstretched
often made better with alcohol intake
pathological hallmarks of parkinson’s?
lewy bodies
loss of dopaminergic neurons from substantia nigra
non-motor symptoms Parkinson’s?
hypomimia
sleep disorders
hallucinations
GI dysfunction (constipation)
bladder problems
depression
congitive imapirment/dementia
anosmia
3 subtypes parkinsons
tremor-dominant (slower rate of progression)
non-tremor dominant (akinetic-rigid syndrome + postural instability gait disorder)
mixed
leadpipe vs cogwheel
Lead pipe = constant resistance throughout passive movement
Cogwheel = jerky resistance throughout movement as muscles contract and relax
Dx Parkinsons
DAT scan (SPECT)

does parkinsons reduce life expectancy?
barely - by 1 or 2 years
greatest risk factor parkinsons?
what decreases risk?
advancing age
smoking and alcohol decreases risk
Tx parkinsons?
levodopa
dopamine agonists
monamine oxidase B inhibitors
amantadine
anticholinergics for tremor
side effects parkinsons Tx?
dopamine agonists
* nausea
* daytime sleepiness
* oedema
* impulse control - gambling, hypersexuality, binge eating, compulsive spending
* hallucinations
levodopa
* greatest symptoamtic benefit but associated with dyskinesia (involuntary movments) and fluctuations in motor symptoms
red flag symptoms PD?
i.e. suggests not Parkinson’s
absence of asymmetry
severe axial or lower limb involvement
frequent falls
eye movement disorder
other unexpected movement disordrs (tics, myoclonus, chorea)
bulbar features
apraxia
severe cognitive deterioration or psychosis
marked autonomic dysfunction
negative levodop challenge
differential diagnoses Parkinson’s?
vascular Parkinsons
drug induced Parkinsons
tremor disorders
multi system atrophy
progressive supranuclear palsy
fragile X tremor ataxia syndrome
vascular parkinsonism features?
Dx?
affects predominantly lower limbs
rest tremor uncommon
poor levodopa response
Dx = brain imaging
drug induced parkinsonism?
symmetrical
coarse postural tremor
presence of other drug-induced disorders - orolingual dyskinesias, tardive dystonia, akathasia
usually narcoleptic/antipsychotic drugs
essential tremor vs parkinsons?
symmetrical, higher frequency (12Hz)
infrequently observed at rest
alcohol responsiveness
head tremor (mild)
multi system atrophy vs parkinsons?
Dx?
core triad = dysautonomia, cerebellar features, parkinsonism
60-70 y/o
jerky postural tremor, pyramidal signs (hyperreflexia and extensor plantar responses)
suboptimal levodopa response
other suggestive features = severe dysarthria/dysphonia, marked antecollis, inspiratory sighing, orofacial dystonia
Dx = MRI “hot cross bun” sign
progressive supraneuclear palsy vs parkinsons
symmetric akinetic-rigid syndrome
predominantly axial involvement
falls
tremor not usually seen
vertical gaze supranuclaer palsy
pseudobulbar symptoms
retrocollis
eyes wide open (staring)
no response to levodopa
fragile X tremor ataxia syndrome (FXTAS) vs Parkinsonism?
late onset (>50 years) neurodegenerative disorder
cerebellar gait ataxia
postural tremor
parkinsonism
dysautonomia
cognitive decline
periperal neuropathy
“where” history brain injury

“where” examination brain injury


CNS
diagnosis = MS

neuromuscular junction problem so either lambert-eaton or myesthenia gravis
lambert eaton = absent deep tendon reflexes
myestheia gravis = hyperreflexia
so Dx = MG

PNS problem
acute = GBS
chronic = diabetes/alcohol
so Dx = GBS
peripheral neuropathy

pseudoathetosis?
Abnormal writhing (usually of fingers) - due to failure of proprioception
Indicates disruption of proprioceptive pathway
bilateral foot drop + high stepping gait
deep fibular nerve

…

…
Guillain barre syndrome
Tx?
progressive paraplegia over days (up to 4 weeks)
sensory symptoms (unlike MND)
pain very common
peak symptoms 10-14 days after onset
post-infectious e.g. campylobacter!
Tx = immunoglobulin infusion, plasma exchange
charcot marie tooth disease?
hereditory sensory motor neuropathy
vasculitis often associated with which neuropathy?
mononeuritis complex
causes of peripheral neuropathy
vasculitis - mononeuritis multiplex
myeloma
hepatitis B/C, HIV, syphillis, Lyme
alcohol
amiodarone, phenytoin, chemo
diabetes
B12/folate deficiency
acute = GBS, porphyria
complication guillain barre syndrome?
autonomic failure (autonomic neuropathy) - cardiac
also respiratory failure
Tx peripheral neuropathy?
treat cause i.e hep C, diabetes
vasculitis = prednisolone + cyclophosphamide
guillain barre = IV immunoglobulin
neuropathic pain relief - gabapentin etc






multiple sclerosis?
most common type?
inflammatory demyelinating disorder in CNS
90% of people will have relapsing remitting MS

clinical features MS?
pyramidal dysfunction (increased tone, hyperreflexia, babinski)
- (extensors = upper limb week, lower limb strong)
- (flexors = upper limb strong, lower limb weak)
optic neuritis
sensory symptoms
urinary tract dysfunction
cerebellar and brainstem features
cognitive impairment
pyramidal dysfunction?
can be symptom of MS
increased tone, spasticity, hyperreflexia, babinski
extensors = weak upper limb, strong lower limb
flexors = strong upper limb, weak lower limb
optic neuritis?
painful vision loss
1-2 weeks
RAPD!!!
cerebellar dysfunction?
(DANISH + PP)
Dysarthria
Ataxia
Nystagmus
Intention tremor
Past pointing
Pendular reflexes
Dysdiadokinesis
internuclear opthalmoplegia?
associated with MS in young people
medial longitudinal fasciculus
lid lag, nystagmus, failure of adduction (diplopia)
urinary tract dysfunction MS?
Frequency
Nocturia
Urgency
Urge incontinence
Retention
Dx MS?
DDx?
at least 2 episodes suggestive of demyelination
MRI (plaques)
CSF (oligoclonal bands)
blood tests to rule out infection, B12/folate deficiency
DDx = mononeuritis complex (vasculitis), structural lesion, infection (syphillis, HIV, borrelia), B12/folate def
Tx MS?
acute exacerbation = steroids (i.e. optic neuritis)
disease modifying therapy = 1st line tecfidera, interferon beta (2nd line monoclonal antibodies, 3rd line stem cell transplant)
symptomatic Tx:
pyramidal dysfunction = baclofen 1st line
sensory = gabapentin/amitriptyline
urge incontinence = oxybutynin
fatigue = amantadine/modafinil
1st line Tx relapsing remitting MS?
tecfidera
40% reduction in relapse rate
lambert eaton myesthenic syndrome (LEMS) associated with?
pathophys?
small cell lung cancer
antibodies to presynaptic calcium channels
myesthenia gravis?
associated with?
autoimmune anitbodies to AChR
association with thymoma
clinical features MG?
Tx?
fatiguable weakness
extraocular, facial + bulbar weakness
limb weakness typically proximal
Tx = pyridostigmine (anticholinesterase), IV immunoglobulin, thymectomy
drug to avoid MG?
gentamicin - makes MG worse
also avoid macrolide antibiotics
muscle power grading?

polymyositis?
Ix?
Tx?
dermatomyositis?
symmetrical, progressive proximal muscle weakness
Ix = raised CK
Tx = steroids
Dermatomyositis
* clinically similar but associated with skin lesions
* Heliotrope rash on face
* 50% have underlying malignancy
commonest muscular dystrophy?
S/s
myotonic dystrophy - autosomal dominant
s/s = myotonia, weakness, cataracts, ptosis, frontal balding, cardiac defects
drugs that can cause myopathies?
statins + corticosteroids
rhabdomyolysis triad?
complications
traid = myalgia, muscle weakness + myoglobinuria
comps = acute renal failure + DIC
traumatic brain injury Tx?
ABCDE
GCS, pupils
check c-spine
head injury severity scale?
Mild = 14 or 15, brief LOC
Moderate = 9-13
Severe = 3-8
NICE guidelines CT scan head injury?
>65 y/o
coagulopathy
RTA or fallen from large height

Dx?

Battle sign = base of skull fracture
Dx?
classical presentation

Epidural haematoma
classic presentation:
Injury with LOC
“Lucid interval”
Deteriorating GCS
hemiparesis
Unilateral fixed and dilated pupil
Apnoea and death
Dx?

acute subdural haematoma

chronic subdural haematoma
Dx?

intracerebral haematoma
Dx?

diffuse axonal injury
Tx raised ICP?
sedation - benzos, propofol
head of bed tilt
mannitol
if all of this fails = decompressive craniectomy
brainstem death?

what MRI sequence do you use for water?
T2 hyperintense
supect haemorrhage?
CT!!
Dx?

subarachnoid haemorrhage
Dx?

diffuse haemorrhage - VERY BAD
Dx?

subdural haematoma with midline shift
extra-axial (outside brain parenchyma) tumours?
meningioma
pituitary adenoma
dermoid/epidermoid tumour
acoustic schwannoma
intra-axial brain tumours?
glioma
glioblastoma
metastases

either metastases or abscesses
chiari malformation?
complication?
s/s?
cerebellum herniates through foramen magnum
complication = can cause obstructive hydrocephalus
S/s = headaches, neck stiffness, seizures etc

cortical dysplasia - presents with seizures

schizencephaly (slit from ventricles)

arachnoid cyst

demyelination - MS
usually see lesions in spinal cord as well

encephalitis
Tx = aciclovir
classification brain tumours?
Supratentorial (usually adults) = above tentorium cerebelli
Infratentorial (usually in children)
Extrinsic (bone, meninges)
Intrinsic (glioblastoma)
presentation brain tumour?
neurological deficit
motor weakness
headache (wakes up from sleep and associated with nausea + vomiting)
seizures
raised ICP triad?
S/s?
cushing’s triad = hypertension, irregular breathing, bradycardia
s/s
- headaches
- vomiting
- mental changes
- seizures
which nerve is most likely to be dysfunctional with tumour?
with uncal herniation?
6th cranial nerve (abducens) most likely to be dysfunctional with tumour
uncal herniation = occulomotor nerve (CN III)
cerebellar examination?
DANISH
Dysdiadokinesia
Ataxia (gait and posture)
Nystagmus
Intention tremor
Slurred, staccato speech
Hypotonia/heel-shin test
investigation of choice for brain tumour?
MRI scan
commonest brain tumour?
metastasis
commonest primary brain tumour?
glioma (glioblastoma)
neuroepithlial tissue?
astrocytes
oligodendroglial cells
epednymal cells/choroid plexus
neuronal cells
pineal cells
astrocytic tumours grading
grade 1 = pilocytic
grade 2 = low grade astrocytoma
grade 3 = anaplastic astrocytoma
grade 4 = glioblastoma multiforme
pilocytic astocytoma?
Affects?
S/s?
Dx?
Tx?
truly benign
affects children
s/s = slow in schooling, walk with tip-toe gait, laughing seizures
Dx = CT
Tx = surgery (curative)

grade 2 astrocytoma found?
presentation?
features on MRI?
temporal lobe, posterior frontal lobe, anterior parietal lobe
presentation = raised ICP, usually seizures
MRI = does not enhance, if it enhances it is a sign it is progressing from grade 2 to grade 3

Tx grade 2 astrocytoma?
surgery + chemo/radiotherapy
prognostic factors grade 2 astrocytoma?
poor prognosis (i.e. will progress to glioblastoma)
- age >45
- low performance score
- large tumours >6cm diameter/crossing midline
malignant astrocytomas?
features?
anaplastic astrocytoma (grade 3)
- medial survival 2 years
glioblastoma multiforme
- most common primary tumour
- median survival <1 year
- multiple gliomas = NF, TS, PML
multiple gliomas a sign of?
neurofibromatosis
tuberous sclerosis
progressive multifocal leukoencephalopathy
Tx grade 3 + 4 astrocytomas?
survival?
non-curative surgery +
post-op radiotherapy +
chemotherapy (temozolamide)
improves median survival to 14 months - so 2 extra months essentially
what else is important to discuss with GBM patient?
must inform DVLA! - seizure risk post-op
side effects radiotherapy brain tumour?
drops IQ by 10
skin changes
hair loss
tired
tiptoeing, ataxia, vomiting + headache in children?
suspect pilocytic astrocytoma
severe headache that wakes from sleep, plus nausea + vom?
suspect brain tumour
meningioma s/s?
associated with?
s/s
- majority asymptomatic
- headache
- cranial nerve neuropathies (CN VI)
Meningiomas associated with - neurofibromatosis type 2, breast cance
classification meningioma?
majority benign
small percentage malignant - clear cell, choroid, rhabdoid, papillary
can also get radiation-induced meningiomas (e.g. after childhood leukemia)
meningioma Dx?
CT - enhancing, skull “blistering”
MRI - dural tail
Angiography - may see occlusion of sagittal sinus

meningioma Tx?
prognosis?
small meningioma = expectant
surgery
radiotherapy
prognosis = 90% 5 year survival
nerve sheath tumours?
schwannomas (aka neruomas)
neurofibromas
acoustic neuromas also called?
what are they associated with?
s/s?
complication?
vestibular schwannomas
associated with neurofibromatosis 2 (suspect in young people with bilateral sesnorineural hearing loss)
s/s
- sensorineural hearing loss
- tinnitus
- vertigo
complication = hydrocephalus
acoustic neuroma Tx?
expectant (hearing aid)
radiation
surgery
if develp hydrocephalus = shunt
normal pressure hydrocephalus s/s?
triad
memory loss + urinary incontinence + ataxic gait
Tx ischaemic stroke?
thrombolysis - IV TPA!!
- limited to <4.5 hours from onset of symptoms
- if >4.5 hours I think you use endovascular therapy
Aspirin 300mg (CT first to exclude bleed, wait 24 hours if thrombolysed)
DVT prevention - LMWH
start statins
Tx haemorrhagic stroke?
anticoagulant reversal
- warfarin = vit K
- dabigatran = idarucizumab
- factor Xa inhibitors = andexanet alpha
- if unavailable = clotting factors
acute spinal cord compression Ax?
Trauma
Tumours - haemorrhage or collapse (vertebrae)
Infection e.g. epidural asbscess
Spontaneous haemorrhage (AVM)
brown sequard syndrome?
ipsilateral motor level
ipsilateral dorsal column sensroy level
contralateral spinothalamic sensory level
central cord syndrome Ax?
S/s?
hyperflexion or extension injury to already stenotic neck (also syringomyelia)
s/s
- distal upper limb weakness
- “cape-like” spinothalamic sensory loss
- lower limb power preserved
- dorsal columns preserved
tumours that can cause spinal cord compression?
extradural
- metastasis from lung, breast, kidney, thyroid etc
intradural
- meningioma, schwannoma
intramedullary
- astrocytoma, ependymoma
Tx spinal trauma?
immobilise
X-ray/CT
MRI to see cord!!
decompress + stabilise
spinal epidural abscess Tx?
antibiotics + surgical drainage
acute spinal cord compression?
EMERGENCY!!!
Parkinson’s Ax?
Risk factors?
5% cases are familial, 95% sporadic
risk factors
- age
- men
- rural living
- (smoking is protective)
drugs that can cause parkinson’s?
Haloperidol - dopamine blockers
Metaclopramide (oncology patients - can get secondary parkinsons)
- And other anti-emetics like prochlorperazine
Ix Parkinson’s?
DAT scan
(test bloods for Wilson’s disease)
Tx Parkinson’s?
L-dopa
Dopamine agonists
Anticholinergics
Amantadine
COMT inhibitors (entacapone)
Apomorphine
analgesic ladder?

which areas of the brain are involved in analgesia?
periaqueductal grey (PAG)
locus ceruleus (pons)
nucleus raphe magnus (medulla)
opoid receptor?
U (mu) - responsible for most of the analgesic action of opioids
major adverse effects of opoids?
respiratory depression - apnoea
orthostatic hypotension
GI - nausea, vomiting, constipation, increased intrabillary pressure
CNS - confusion, hallucinations, dizziness, hyperalgesia (with excessive use)
what drug should be avoided with pethidine?
MAO inhibitors
tramadol avoided in?
patients with epilepsy
1st line treatment for trigeminal neuralgia?
carbamazepine
allodynia?
hyperalgesia?
Allodynia = pain from stimulus that is not normally painful e.g. cotton wool
Hyperalgesia = more pain than expected from a painful stimulus e.g. pin prick
Tx neuropathic pain?
Tricyclic antidepressants
Anticonvulsants\opioids
NMDA antagonists e.g. ketamine
Sodium channel blockers e.g. lignocaine
Capsaicin
GABA agonists (e.g. Baclofen)
MS?
Dx?
Autoimmune demyelinating disorder characterised by distinct episodes of neurological deficit, separated in time, and which correspond to spatially separated foci of neurological injury
Clinical diagnosis
- 2 distinct neurological deficits occurring at different times
- Multiple distinct (usually white matter) CNS lesions on MRI
Diagnosis can also be backed up by
- IgG oligoclonal bands in CSF
- MRI showing demylinated plaques
Dx?

MS
clinical features MS?
Typically presents with focal neurological deficit
- Optic nerve lesions (optic neuritis)
- Unilateral visual impairment
- Spinal cord lesions
- Motor/sensory deficit in trunk and limbs
- Spasticity
- Bladder dysfunction
- Brain stem lesions
- Cranial nerve signs
- Ataxia
- Nystagmus
- Internuclear ophthalmoplegia
types MS?
Clinically isolated syndrome
Relapsing and remitting (most common)
Secondary progressive
Primary progressive
risk of passing MS to child?
approx 5%
dementia classification?
most common types?
most common types = alzhiemer’s disease + vascular dementia

death Alzhiemer’s?
usually occurs due to secodary cause such as bronchopneumonia
microscopic features Alzheimers?
plauques - amyloid angiopathy (amyloid AB)
neurofibrillary tangles (tau protein)
risk factors Alzhiemer’s?
AGE
Down’s syndrome
presnillin 1 and 2
Apolipoprotein E
amyloid angiopathy Dx?
Comp?
Stains with congo red - bright green
comp = intracerebral haemorrhage
Tx Alzhiemer’s?
Anticholinesterase drugs (cholinesterase inhibitors)
- e.g. donepezil, galantamine, rivastigmine
NMDA receptor blockers - memantine
Lewy body dementia clinical features?
contrast with Alzheimers?
pathophys?
Dx?
Clinical features
- Progressive dementia
- hallucinations and fluctuating levels of attention/cognition
- REM sleep behaviour disorder (acting out dreams)
- Parkinsonism
in contrast to Alzhiemers, memory affected later
pathophys = degeneration of substantia nigra (like Parkinson’s) + lewy bodies
Dx = lewy bodies + amyloid in brain

Parkinsonism seen in which conditions?
Idiopathic parkinson’s disease
Lewy body dementia
Drugs e.g. phenothiazines
Trauma e.g. dementia pugilistica
Multi-system atrophy (nystagmus)
Progressive supranuclear palsy
Cortico-basal degeneration
macroscopic finding Huntington’s?
atrophy of caudate nucleus
Front-temporal dementia (Pick’s disease)?
S/s?
Progressive dementia commencing in middle life (50-60) characterised by progresive changes in personality + behaviour
S/s
- Personality and behavioural change
- Speech and communication problems
- Changes in eating habits
- Reduced attention span
histological hallmarks FTD?
Pick’s cells (swollen neurons)
Pick’s bodies

Multi-infarct dementia (vascular dementia)?
distinguish from Alzhiemer’s?
Dx?
Tx?
Cumulative damage to brain through hypoxia as result of multiple blood clots in brain
distinguish from alzheimers = abrupt onset, stepwise progression
Dx = history of stroke/HTN, evidence of stroke on CT/MRI
Tx = cannot reverse damage that’s already happened
- aim to prevent further strokes
- lifestyle
- statins
- BP
- Warfarin
Dx?
clinical features?
Ax?
triggering factors?

Dx = transient global amnesia
clinical features
- anterograde>retrograde amnesia (repetitive)
- abrupt onset
- preserved knowledge of self - they know name, DOB
- always <24 hours!!
Ax = unknown
Triggering factors = emotion/changes in temperature
Dx?
S/s?
Tx?

Dx = transient epileptic amnesia
S/s
- short-lived
- forgetful/repetative questioning
- can carry out complex activities with no recollection of events
Tx = AEDs

prion disease i.e. CJD
Dx?
s/s?
Ix?
pathophys?
Tx?

Dx = limbic encephalitis
s/s = short term memory loss, seizures, behavioral change
Ix = anti-Hu antibodies
pathophys = underlying malignancy or autoimmune
Tx = treat tumour/immunosuppressants
early onset AD?
<65 y/o, may have genetic influences
Ix Alzheimers?
cognitive tests
MRI - frontal + temporal lobe atrophy
SPECT - decreased temperoparietal metabolism
CSF - decreased amyloid, increase tau protein
Dx?
Features?
S/s?
Ax?

frontotemporal dementia
early onset <65 + Pick bodies
s/s
- personality + behavioural changes
- disinhibition, loss of empathy, hyperorality (can’t stop eating) and other addictive behaviours (online shopping)
- early loss of insight (collateral history vital)
25% genetic cause - c9orf
Ix FTD?
Tx?
MRI - trophy of frontal and temporal lobes
SPECT - decreased frontotemporal mentabolism
CSF - increased TAU but normal amyloid
Tx
- trazadone/antipsychotics
- safety management - controlled acess to food, money, internet
- power of attorney
vascular dementia onset?
core cliical features?
s/s?
Ax?
prognosis?
Tx?
late onset dementia >65 y/o
core clinical features = prescence of cerebrovascular disease + clear temporal relationship between dementia and cerebrovascular disease
s/s = decreased attention, executive dysfucntion, slowed processing
Ax = can be after stroke (easy), or small vessel disease (more difficult to prove)
prognosis same as Alzhiemers - ~8 years
Tx = reduce vascular risk factors + cholinesterase inhibitor
lewy body dementia onset?
Ax?
core clinical features?
late onset >65 y/o
Ax = a-synuclein builds up and damages cells - causes disruption to cholinergic (memory) and dopaminergic pathways (parkinsonism)
clinical features = fluctuating cognition + visual hallucinations + extrapyramidal features (bradykinesia, rigidity, tremor)
Ix Lewy Body dementia?
Tx?
Ix
- DAT scan
- diagnostic = a-synuclein in CSF/a-synucliein ligand imaging
Tx
- levodopa
- cholinesterase inhibitors
- support - community nurse

Parkinson’s disease dementia?
how to differentiate from lewy body?
s/s?
Tx?
late onset >65 y/o - occurs after 20 years of Parkinson’s
DLB <1 year presentation
PDD >1 year presentation
s/s
- parkinson’s (bradykinesia, rigidity, temor)
- dementia (decreased attention, impaired visuospatial function + memory)
Tx = same as DLB
- levodopa + cholinesterase inhibitor
Huntington’s disease dementia?
s/s?
Ix?
Tx?
early onset dementia (30-50 y/o)
s/s
- changes in mood/personality
- chorea
- impaiment of memory
- psychosis
Ix = genetic testing + MRI (loss of caudate heads)
Tx = mood stabilisers, drugs that suppress chorea
proteinopathy associated with:
Alzhiemer’s?
vascular dementia?
Parkinson’s disease dementia?
Lewy body dementia?
CJD?
FTD?
Huntington’s?
Alzhiemer’s = amyloid
Vascular dementia = amyloid
PDD = a-synucluein
DLB = a-synuclein
CJD = prion
FTD = tau protein
HD = Huntingtin
REM parasomnia associated with?
Parkinson’s disease - will act out dreams
Narcolepsy pathophys?
s/s?
pathophys is unknown, usually begins as teenager
Daytime sleepiness
- Involuntary somnolence during eating/talking
Cataplexy - loss of muscle tone triggered by emotion
Hypnagogic hallucinations (occur at sleep onset)
Sleep paralysis
RBD - act out dreams
Ix narcolepsy?
overnight polysomnography
multiple sleep latency test
origin of corticospinal tract?
parts?

corticobulbar tract origins?
Function?
what does it innervate?

eyebrow raise sign?
forehead sparing = LMN lesion
non-forehead sparing = UMN lesion

rubrospinal tract originates from?
Function?

reticulospinal tract originates from?
Function?

which tract is active in decortiate rigidity?
decerebrate rigidity?
decorticate = rubrospinal tract still active
decerebrate = reticulospinal tract still active

lesion in blue line?
red line?

blue line = both rubrospinal and reticulospinal tracts active
red line = reticulospinal tract still active

…
central cord syndrome associated with?
disruption fo which tracts?
s/s?
syringomyelia
disrpution of corticospinal and spinothalamic tract
s/s
- cape-like loss of pain and temperature
- weakness and spasticity in upper limbs (worse than lower limbs)
anterior cord syndrome disrupts which tracts?
all tracts except DCML

syringomyelia
what is syringomyelia associated with?
arnold chiari malformation
where are sinuses in brain found?
dura mater

…
diagnostic tests SAH?
CT angiogram then LP (blood)

1 - subdural
2 - SAH
3 - extradural

…
Dx?
associated features?

SAH
meningeal irritation can cause neck stiffness and photophobia
symptoms cerebral herniation?
UMN signs - spatic paralysis, brisk reflex, upgoing plantars
Cushing’s triad (ICP) - HTN, bradycrdia + irregular breathing
unreative pupil (uncal hernation - CN III)
Cushing’s triad?
signs of raised ICP
hypertension + bradycardia + irregular breathing

degenerative cervical myelopathy

1 - lumbar stenosis
2 - cauda equina
3 - mechanical back pain

…
vascular territories of brain?

anterior circulation stroke?
dysphasia
homonymous visual field defect
contralateral motor/sensory deficit of at least 2 areas (out of face, arm, leg)
posterior circulation stroke?
cerebellar dysfunction (ataxia, dysdiadokinesia, nystagmus, intention tremor, slurred speech, heel-shin)
isolated homonymous vidual field defect
cranial nerve dysfunction
lacunar stroke?
pure motor or pure sensory stroke

1 - lacunar stroke
2 - partial anterior stroke
3 - posterior stroke

…

brocas = 2
wernicke’s = 4
cerebellum = 6

1 - cerebellum
2 - right temporal lobe
3 - left parietal lobe (numbers + writing)
most common cause of non-communicating hydrocephalus?
cerebral aqueduct obstruction


non-communicating hydrocephalus due to aqueduct stenosis

normal pressure hydrocephalus
triad normal pressure hydrocephalus?
gait disturbance + mild dementia + impaired bladder control
Intracerebral haemorrhage Ax?
Ix?
Ax = trauma, hypertension, tumour, AVM, aneurysm, venous cavernoma, haemorrhagic stroke, venous sinus thrombosis
Ix
- ABCDE
- HPC
- PMHx - anticoahulation? liver dysfunction? previous stroke? malignancy?
s/s intracerebral haemorrhage?
Global
- Headache
- N + V
- Reduced GCS
- Pupils
- → raised ICP
Focal
- Paresis
- Dysphasia
- Numbness
- Seizure
- Visual symptoms
- Cerebellar symptoms
Associated problems
- SAH - photophobia, meningism
- IVH - hydrocephalus (raised ICP)
- Trauma - external trauma
Dx intracerebral haemorrhage?
AVM?
aneurysms?
non-contrast CT
AVM = CTA
aneurysms = DSA (digital subtraction angiography)

…
Tx subdural haematoma?
reduce ICP (sit patient up?) correct clotting
control BP
surgery
cerebral perfusion pressure equation?
CPP = MAP - ICP

what is major determinant of CPP?
ICP
effect of CO2/lactic acid on cerebral arterioles?
dilate!!!
Increased CO2/increased BP → vasodilation
Decreased CO2/decreased BP → vasoconstriction
Ax raised ICP?
SOL - tumour, haematoma, asbscess
brain swelling - liver failure, encephalopathy, hypercarbia
increased centrla venosu pressure - venous sinus thrombosis, obsruction of juglar veins
causes of hydrocephalus

normal ICP?
7-15 mmHg
(lower in children)
s/s raised ICP?
Early signs (worst hangover ever)
- Reduced level of consciousness
- Headache
- Pupillary dysfunction +/- papilloedema
- Changes in vision
- Nausea and vomiting
Later signs
- Coma
- Fixed, dilated pupils
- Hemiplegia
- Bradycardia → cushing’s triad
- Hyperthermia
- Increased urinary output
Tx ICP?
- Maintain head in midline (at 30-45 degrees elevation) to facilitate blood flow
- Loosen collars etc
- Avoid gagging, coughing
- Treat hyperthermia
- Maintain fluid balance and normal electrolytes
- Maintain normocarbia
Tx hydrocephalus?
Use diuretics (mannitol, furosemide)
Barbiturate coma
Antiepileptics
Surgical decompression (shunt?)

arnold chiari malformation
(cause of obstructive hydrocephalus)
Ix?

CT - DO NOT LP!!!
Tx non-communicating hydrocephalus?
ventriculoperitoneal shunt
Hakim’s triad?
normal pressure hydrocephalus
abnormal gait, urinary incontinence, and dementia
Dx?

normal pressur ehydrocephalus - lateral sulcus is much thicker than sagittal
Ax normal pressure hydrocephalus?
Ix?
Tx?
Ax - uncertain (can be due to venous sinus stenosis)
Ix
- LP (remember not in other causes of hydrocephalus)
Tx
- VP shunt
- Medium or low pressure valve
idiopathic intracranial hypertension?
features?
S/s?
Raised intracranial pressure of unknown cause
features = no ventricular dilation, mainly women of child-bearing age, obese
s/s
- headache
- double vision + visual blurring
- tinnitus
- radicular pain
- papilloedema

Ix idiopathic intracranial hypertension?
Tx?
Ix
- LP
- CT/MR head
- CTV!! (venous pressure possible cause)
- Fundoscopy + ophthalmology review
Tx
- weight loss
- carbonic anhydrase inhibitors (acetazolamide, topiramate)
- diuretics
- intracranial venous sinus stenting
cervical myelopathy symptoms?
Tx?
s/s
- clumsiness in hands
- gait imbalance
- numbness, tingling
- neck pain and stiffness
- UMN sings - brisk reflexes, babinski
- hoffman’s sign
Tx = surgery!!
most likely cause of non-communicating hydrocephalus in teenager?
6 month old?
arnold chiary presents in teenage years
aqueduct stenosis is congenital so would cause non-communicating hydrocephalus in 6 month old
56 y/o man, headache 8/10, nausea + vomiting, ptosis, bilaterally constricted pupils
horner’s syndrome due to ICA dissection
56 y/o man presents with progressive headache, 6/10 severity, right dilated unreactive eye
posterior communicating artery aneurysm
10/10 severity headache, neck stiffness and photophobia
SAH!!
Dx?

Periventricular white matter is very dark
Asymmetrical
Myelin is reason its white
So these are demyelinating plaques - multiple sclerosis
UMN pattern of weakness?
Ax?
how to determine site?
pyramidal/corticospinal = weak extensors in arm, weak flexors in leg
Ax
- stroke, SOLs, spinal cord lesions
determine site
- hemispheric = contralteral pyramidal weakness in face, arm, leg
- parasagittal frontal lobe lesion = paraparesis
- spinal cord = pyramidal weakness below level of lesion
- cervical = arms + legs
- throacolumbar = legs
Ax LMN signs?
Motor neuron disease
Spinal muscular atrophy
Lead poisoning, poliomyelitis etc

…

…
neuromuscular junction s/s?
Ax?
how to differentiate
Neuromuscular junction = fatigable weakness, normal or decreased tone - no sensory symptoms!!
Ax = MG or Lambert Eaton
- MG = have hyperreflexia
- LEMS = absent reflexes
patterns of sensory loss?


…
cerebellar signs?
Cerebellar gait is broad-based and unsteady
Intention tremor + ataxia
Dysdiadochokinesia
Nystagmus and dysarthria are additional features
s/s frontal lobe damage?
- Personality dysfunction - disinhibition, apathy
- Paraparesis
- Paratonia (inability to relax muscles)
- Grasp reflex
- Frontal gait dysfunction (magnetic gait)
- Cortical hand
- Seizures
- Incontinence
- Visual field defects (optic chiasm beneath frontal lobe)
- Expressive dysphasia (Broca’s area in frontal lobe)
- Anosmia (olfactory pathway beneath frontal lobes)
s/s temporal lobe damage?
- Memory dysfunction - episodic memory
- Agnosia (visual and sensory)
- Receptive dysphasia (Wernicke)
- Visual field defects (upper homonymous quadrantanopia)
- Auditory dysfunction (Heschel’s gyrus)
- Limbic dysfunction
- Temporal lobe epilepsy
parietal lobe damage s/s?
Visual field defect (lower homonymous quadrantanopia)
Sensory dysfunction (visual and sensory)
Gerstmann’s syndrome - dysgraphia, left-right disorientation, finger agnosia, alcalculia
Dyspraxia
Inattention
Ix MS?
MRI with gadolinium contrast
oligoclonal bands in CSF
acute relapse MS Tx?
steroids