NEURO Flashcards
what is a dermatome
area of skin supplied by single spinal nerve
what is a myotome
volume of muscle supplied by single spinal nerve
what is a somite
brick like block on embryo
each form single spinal nerve which gives skin and muscle of each segment individual supply = forms dermatomes and myotomes
what is anencephaly
failure of fusion of neural tube at cranial end
what is spina bifida
failure of fusion of neural tube at caudal end
at what level is a lumbar puncture performed
L3-L4 / L4-L5
performed further down from conus medullaris/corda equina as less likely to cause spinal damage
what are the 3 layers of the meninges
dura = firmly adhered to the skull
arachnoid = adhered to the brain
pia = attached to brain cannot be separated
what is horner’s syndrome
lesion of sympathetic supply
typically causes small pupils, ptosis, anhidrosis
how does a lesion of cerebral hemispheres typically present
unilateral affects the contralateral side
how does a lesion of the internal capsule typically present
complete contralateral hemiparesis
how does a lesion of the spinal cord typically present
bilateral
typically affects legs
often bladder involvement
how does a lesion of the cerebellum typically present
ataxia
loss of coordination
how does a lesion of the brain stem typically present
bilateral weakness
bulbar involvement
cranial nerve nuclei commonly affected
how does a lesion of the peripheral nerves typically present
gloves and stocking appearance
what are the 3 branches of the aortic arch
right brachiocephalic trunk
left common carotid
left subclavian
at what level does the common carotid artery bifurcate
C3/4
what are the 4 parts of the internal carotid artery
cervical
petrous
cavernous
supraclinoid
what do the extracranial vertabral arteries supply
neck muscles
cervical spine meninges
cervical spinal cord
what are the branches of the intercranial vertebral arteries
posterior inferior cerebellar artery
anterior spinal artery
small medullary perforators
what are the branches of the basilar artery
posterior cerebral arteries
superior cerebellar arteries
anterior inferior cerebellar arteries
pontine perforators
where does the posterior inferior cerebellar artery arise from
terminal bifurcation of the basilar artery
what does OTOMCAT stand for
in carotid sinus:
occulomotor nerve
trochlear nerve
opthalmic division of trigeminal
maxillary division of trigeminal
cavernous segment of internal carotid
abducens nerve
trochlear nerve
which nerves run through the carotid sinus
occulomotor 3
trochlear 4
opthalmic V1
maxillary V2
abducens 6
what are the main types of primary headache
cluster
tension
migraine
trigeminal neuralgia
what are the main types of secondary headache
subarachnoid haemorrhage
menignitis
encephalitis
idiopathic intercranial hypertension
giant cell arteritis
drug overdose
what signs/symptoms suggest a possible secondary headache
Hx of HIV/cancer
vomiting without cause
changing personality/cognitive dysfunction
jaw claudication
severe eye pain
what symptoms of headache are considered to be red flags
new headache with history of cancer
thunderclap headache = SAH assume
seizure
significantly altered consciousness, memory, confusion, coordination
papilloedema
abnormal neuro exam or symptom
what are red flags during a clinical headache examination
fever
altered conciousness
neck stiffness/kernigs sign
focal neurological signs
ALWAYS CHECK BP
how does idiopathic intercranial hypertension present
pain is worse on waking, coughing, sneezing, straining, lying down
presents with nausea/vomiting
papilloedema may present
name 5 bacterial causes of menigitis
neisseria meningitidis
strep. pneumoniae
listeria monocytogenes
E.coli
group B strep
(strep agalactiae = neonates)
name 4 viral causes of meningitis
enterovirus
mumps
herpes simplex
varicella zoster
when should a lumbar puncture NOT be performed in suspected meningitis
if intracranial pressure is raised
if petechial rash is present
if patient has abnormal clotting
what is the prophylaxis for meningitis
ciprofloxacin (close contacts)
rifampicin
what is the first line treatment for any suspected meningitis
IV Benzylpenicillin
what is the treatment for bacterial meningitis
cefotaxime OR ceftriaxone AND dexamethasone
possible add:
chloramphenical (peni allergy)
amoxicillin (immunocomp)
vancomycin (recent travel)
what is the treatment for encephalitis
acyclovir in case its herpes simplex virus
what is the most common cause of encephalitis
herpes simplex virus
what spores cause tetanus
clostridium tetani
what toxins do clostridium tetani spores produced
tetanolysin and tetanospasmin = cause tissue lysis and spasms
what drug is used to treat tetanus
metranidazole
describe the furious stage of rabies
agitated
hydrophobia
aerophobia
hyperactivity
describe the paralytic phase of rabies
flaccid
weakness
not really there
how is rabies managed
high does sedatives = end of life care
vaccination for pre-exposure prophylaxis
Ig for post exposure prophylaxis
what is herpes zoster
viral disease characterised by painful skin rashes with blisters in localised areas
describe the pathophysiology of herpes zoster
caused by reactivation of varicella zoster virus which may remain inactive within nerve cells
when reactivate = travel down nerve cells and effects dermatome its present in
how does herpes zoster present
headache
pyrexia
malaise
burning pain
itching
hyperesthesia (extra sensitive)
parasthesia
how is herpes zoster treated
analgesia = paracetamol, ibuprofen, opiates, topical capsaicin, topical lidocaine, gabapentin
antivirals = acyclovir
what mediates the demyelination in MS
macrophages
what are the 3 types of MS
relapse remitting MS
primary progressive MS
secondary progressive MS
what is the Lhermitte’s sign
electric shock sensation down spinal cord on movement of head
SEEN IN MS
what would be seen on an MS MRI
plaques of focal demyelination
what is an epileptic seizure
paroxymal event in which excessive hypersynchronous neuronal discharges in brain cause change in behaviour sensation or cognitive processes
what are the differentials for an epileptic seizure
syncope
non-epileptic seizure
migraine
hyperventilation
TIA
what is syncope
insufficient blood/oxygen to brain
caused by sitting or standing
rarely from sleep
5-30s duration
rapid post ical recovery
what is a non epileptic seizure
caused by psychosocial stress
1-20 min duration
closed eyes/mouth or crying/speaking
what would suggest epilepsy over syncope
tongue biting
head turning
muscle pain
loss of consciousness more than 5 mins
cyanosis
what would suggest syncope over epilepsy
prolonged upright position
sweating prior
nausea
presyncopal symptoms
pallor
how do you differentiate between NES and epileptic seizures
CANT use history
video of seizures needed
what is obstructive/non communicating hydrocephalus
blockage of ventricles = CSF buildup due to lack of drainage
what can cause obstructive hydrocephalus
foreign material in CSF
tumours compressing outflow tract
posterior fossa pathology
how does obstructive hydrocephalus present
headaches
seizures
vomiting
downward eyes
loss of coordination
incontinence
what is normal pressure hydrocephalus
intermittent increasing of ICP
how does normal pressure hydrocephalus present
incontinence
dementia
falls
wide gait
magnetic gait = stuck to floor
how is normal pressure hydrocephalus treated
shunt placement = drains extra fluid from ventricles to peritoneum
what is cerebellar syndrome
ataxia and nystagmus due to cerebellar injury
appear/feel drunk
deficit is IPSILateral
caused by stroke/tumours/haemorrhage
what is jugular foramen syndrome
glossopharyngeal, vagus, accessory palsies present
reticular activation system maybe also affected
what is the reticular activation system
involved in:
alertness
sleeping
waking
respiration
cardiovascular drive
what is the difference between focal and generalised seizures
focal = occur in one part of brain
generalised = affect whole brain
what are the 2 different types of focal seizures
without impaired consc = no post-ictal sympt
with impaired consc = most commonly temporal lobe
what is an obvious feature of 3rd nerve palsy
down and out pupil
what would 3rd nerve palsy with pupil dilation suggest
space occupying lesion compressing nerve
what is the effect of brown-sequard syndrome
lesion in spinal cord causes hemisection of spinal cord:
SPINOTHALAMIC = contralateral loss of pain, temp, crude touch, pressure 2 levels below lesion
DCML = ipsilateral loss of fine touch, proprioception, vibration (decussation in medulla)
DESCENDING TRACTS = ipsilateral hemiparesis/spastic paralysis below lesion
LMN = ipsilateral loss of sensation and flaccid paralysis at level of lesion
what neurological conditions are vaccine preventable
polio
tetanus
TB
H.influenzae
measles
meningococcus
what is clinical epidemiology
uses information about distribution and determinants in a clinical setting, especially in diagnosis
what is incidence
how many cases each year
what is the prevalence
proportion of population affected
what is the burden of disease
time lost off work
describe the use of epidemiology in neural disease
- case ascertainment
- incidence/prevalence/trends
- risk factors
- scope for earlier diagnosis and prevention
what are the public health risk factors for migraine
age, sex, FHx = female more common
education/income
oral contraceptives
what are the public health risk factors of stroke
age, sex = male more common
hypertension
cardiac disease, DM
smoking/alcohol
describe the rehabilitation following a stroke
84% return home but not necessarily back to work
what public health interventions are there for dementia
opportunistic screening for memory loss in NHS health checks
dementia controversial
what are the risk factors for cerebral palsy
anoxia
low birth weight
which neurological conditions are of public health importance
migraine
stroke
dementia
epilepsy
parkinsons
MS
cerebral palsy
describe the prevalence of MS
directly proportional to distance from equator
uncommon in fishing communities
positive association with some HLA antigens
what is Creutz-Jakob disease (CJD)
rapidly progressive dementia = very rare
14% associated with gene mutation
how is head injury classified
type = penetrative/blunt
lesion distribution = focal or diffuse
time course = primary (immediate), secondary (effect after injury
what is a contusion injury
due to blow of force
essentially brain ‘bruises’
occur at site of injury = coup
occur away from site of injury = contrecoup
what is a laceration
blow to head lead to tear in tissues (pia mater)
what is a diffuse traumatic axonal injury
injury to axons due to trauma that occurs throughout the brain
pattern of tears
usually involves acceleration and deceleration of head
describe the recovery of mild traumatic axonal injury
recovery of consciousness
may be longterm
variable severity deficit
describe the recovery of severe traumatic axonal injury
unconscious from impact and remain so/severe disability
what is the prognosis for diffuse vascular injury
usually result in near immediate death
multiple petechial haemorrhages throughout brain
what can cause brain swelling
congestive brain swelling
vasogenic oedema = fluid leaves damaged blood vessels
cytotoxic oedema = increase water in neurons/glia
what is hypoxia-ischaemia
lack of oxygen and blood to brain
can be diffuse or focal
results in increased intercranial pressure
what is chronic traumatic encephalopathy
repetitive low-level blows to the head with or without loss of consciousness which cause neurological deficit later in life
how does chronic traumatic encephalopathy present
after injury =
personality change
epilepsy
memory issues
later life = parkinsonism
what is weakness/paresis
impaired ability to move body part in response to will
what is paralysis
no ability to move body part in response to will
what is ataxia
willed movements = clumsy and uncontrolled
what is apraxia
disorder of consciously organised patterns of movement or impaired ability to recall acquired motor skills
where are lower motor neurones found
cranial nerve nuclei in the brainstem
anterior horn on spinal cord
describe the final common pathway
LMN then along axon then to neuromuscular junction then to muscle fibres
what is a motor unit
basic functional unit of muscle activity
includes LMN, axon and several supplied muscle fibres
what controls muscle tone
stretch receptors detect stretch (afferent nerves)
gamma motor neurons innervate stretch receptors to allow for contraction
what is muscle tone
resistance of muscles to stretch
what are the clinical features of LOWER MN disease
= everything goes DOWN
muscle tone reduce
muscle wasting
fasciculation = twitching
reflexes depressed or absent
focal weakness
absent bobinski sign
name 5 causes of lower MN lesions
polio
guillain-barre syndrome
ALS (motor neurone disease)
myasthenia gravis
vascular disease
how are lower motor neurone disease investigated
neurophysiology nerve conduction sites
brain and spinal MRI
lumbar puncture
bloods = muscle enzymes, auto-antibodies, peripheral neuropathy screen
what are the clinical features of UPPER MN leasions
= everything up
muscle tone increased
tendon reflexes/jaw jerk
positive bobinski sign
characteristic pattern of muscle weakness (pyramidal)
emotional liability
describe the pyramidal characteristic pattern of weakness seen in UMN lesions
legs = weaker flexors than extensors
arms = weaker extensors than flexors
name 7 causes of UPPER MN lesions
stroke
brain injury
spinal cord injury
cerebral palsy
MS
MND/ALS
CNS tumour
how are upper MN lesions investigated
LP
Bloods for metabolic disorders
MRI brain/spine
what increases chance of brain tunours
ionising radiation
family Hx (for gliomas)
immunosuppression
history of cancer
where do primary brain tumours arise from (5)
- germ cell line = craniopharyngioma or medulloblastoma = in children (WHO grade 4)
- meninges = meningioma, usually benign (WHO grade 1)
- sella region = pituitary adenoma
- glial cells = glioma usually astrocytoma/oligodendroglioma (WHO grade 2)
- cranial nerves = schwannomas
which primary tumours commonly metastasise to the CNS
BLT CRM
breast
lung
testicular
colorectal
renal
malignant melanoma
how are brain tumours classified
WHO classification based on histology
I = most benign
4= most malignant
how do low grade gliomas present (I-II)
slow growing
allo pathways to move so less deficit
commonly present with seizures
how do high grade gliomas present (III-IV)
rapidly progress so = neurological deficit
symptoms of raised ICP and focal/non focal neurology
what type of brain tumour presents more commonly with seizures
low grade tumours
what are functional symptoms
disorder of function and not structure
structure is normal
what are organic symptoms
some kind of structural issue with the body
can be detected by physical exam or test
what is somatisation
converting emotions into physical signs
what is dissociation
dissociating immediate reality into alternate reality
how does cerebellar disease present
ataxia
nystagmus
dysarthria (slurred/slow speech)
dysdiadochokinesia
intention tremor
what is dysdiadochokinesia
inability to perform rapid repetitive tasks
what cells are lost in ataxia of the cerebellum
purkinje cells
what is nystagmus
rapid uncontrolled movement of eyes in one direction
most noticeable looking TOWARDS the lesion
describe the classification for the severity of ataxia
mild = mobilise independently or with 1 walking aid
moderate = mobilise with 2 walking aids or frame
severe = mostly wheelchair bound
what is the name of ataxia classification
scale for assessment and rating of ataxia (SARA)
how is ataxia investigated
head MRI = first choice
FBC, U+E, vitamin B12
genetic testing
what does a hot cross bun sign on the pons on brain MRI indicate
multisystem atrophy cerebellar type MSA-C
what causes cerebellar disease
- tumours
posterior circulation stroke
haemorrhage
head trauma - VZV
- alcoholism
heavy metal poisoning - Friedrich ataxia (autosomal recessive)
Wilsons disease (excess copper)
what causes ataxia (6)
- cerebrovascular damage = post. circulation stroke
- primary/secondary tumours
- hydrocephalus
- MS
- familial ataxia
- idiopathic ataxia
what is kernigs sign and in what condition would you expect to see it
cannot straighten leg past 130 degrees (hip is flexed at 90 degrees but leg cannot extend further without pain)
subarachnoid haemorrhage or meningitis
which is the dominant brain hemisphere for language and speech
left hemisphere
what is the ABCD2 score used for
assess risk of further stroke following a TIA
high risk = 4 points or more
describe the ABCD score
age = 60+
BP = 140/90 +
clinical features = unilateral weakness/speech problems
durations = 60 mins +
diabetes
what makes a TIA high risk
ABCD 4 points or more
atrial fibrillation
more than 1 TIA in 1 week
TIA whilst on anticoagulant
name 8 causes of raised intercranial pressure
- tumours
- head injury
- haemorrhage
- meningitis
- encephalitis
- brain abcess
- hydrocephalus
- cerebral oedema
describe the pathophysiology of raised ICP in 6 steps
- brain compensates = less CSF/more drainage
- compensation exhausted = ICP starts to increase
- displacement/distortion of brain structures including midline shift
- pressure on occulomotor = down+out+dilated pupil
- ICP continues to increase = cerebellar tonsils herniate through foramen magnum + midline bleeding of brainstem
- DEATH
how does raised ICP present
headache = worse on coughing/leaning forward
vomiting/nausea
altered GCS
decrease HR, increased BP
pupillary changes
papilloedema
Cheyne-stokes respiration
what is cheyne-stokes respiration
periods of apnoea followed by increased breath then decreasing breaths
how is ICP investigated
head CT
blood pressure
lumbar puncture EXCEPT in suspected mass lesions as this can cause brain herniation and DEATH
how is raised ICP treated
hyperventilation = decrease pCO2 = cause cerebral vasoconstriction
craniotomy/burr holes (definitive treatment)
treat cause
what is an essential tremor
gradual onset and worsening of intention tremor
how is essential tremor different from intention tremor
essential at rest
essential are present without associated symptoms
essential effects hands, head/voice, paarkinsons = whole body
intention = present when moving arm e.g. anxiety
how are essential tremors treated
beta blockers (not in asthma)
primidone = antiepileptic
gabapentin = antiepileptic
deep brain stimulation
what is huntingtons disease
autosomal dominant neurodegenerative disorder caused by lack of neurotransmitter GABA
decreased GABA and ACh
increased dopamine
what causes huntingtons disease
repeated CAG sequence
over generations repeat increases = called anticipation = earlier age of onset withe more CAG sequences
caused by HTT gene
how does huntingtons present
psychiatric = irritability, depression, anxiety
chorea = jerky, dance-like rigid movements, stop in sleep
dementia
dysarthria = unclear speech
dysphagia
incoordination
seizures
abnornmal eye movement
how is huntingtons diagnosed
mainly clinical with FHx
head CT/MRI shows caudate nucleus atrophy and increase size of ventricles
genetic testing shows CAG sequence repetition or presence of HTT gene
what parts of the brain reduce in size in huntingtons
caudate nucleus and putamen
how is huntingtons managed
no cure, just prevent progression
reduce chorea
= RISPERIDONE dopamine receptor agonist)
= benzodiazepines
= dopamine depletion (tetrabenazine)
antidepressants = SSRIs
antipsychotics = neuroleptics (haloperidol)
genetic counselling
what signal do A alpha fibers send
= large myelinated fibres
proprioception
whats signal do A beta fibres send
= large myelinated fibres
light touch
pressure
vibration
what signal do A gamma fibres send
= thin myelinated
pain and cold sensation
what signals do C fibres send
= thin, unmyelinated
pain and warm sensation (this is why burning sensation is painful)
when is ataxia caused by a sensory neuropathy
when ataxia gets worse when eyes closed or dark
what is guillain barre syndrome
rapid onset muscle weakness caused by autoimmune damage to peripheral NS schwann cells
what causes guillain barre
3-6months after infection
campylobacter jejuni or cytomegalovirus most common
how does guillain barre present?
intially = numbness/tingling/pain
then = rapid bilateral muscle paralysis
cranial nerve involvement (facial) = weak face, dysphasia/dysarthria, weak eye muscles
back pain
muscle pain
absent reflexes
in severe cases of guillain-barre what can muscle weakness lead to
respiratory failure
how is guillain barre diagnosed
- clinical
- lumbar puncture = elevated protein, low/normal WBC
- nerve conduction studies = most useful
- spinal MRI to exclude lesions
how is guillain barre treated (6)
- IV immunoglobulins = neutralise harmful antibodies
- plasmapharesis = filters out antigens from blood
- intubation for resp failure
- analgesia
- occupational therapy/social work/physical therapy/psychologists
(6. possible DVT prophylaxis due to immobility)
what are the 2 areas a stroke can affect
anterior circulation = circle of willis and branches
posterior circulation = basilar artery and branches
what is thrombolysis
given intravenously to break up clot
give up to 4.5 hours post onset of symptoms
what are the contraindications for thrombolysis (8)
- recent surgery
- recent arterial puncture
- active malignancy
- evidence of brain aneurysm
- anticoagulants
- severe liver disease
- acute pancreatitis
- clotting disorder
what are 2 key findings that suggest a subarachnoid haemorrhage
thunderclap headache = sudden onset
star shape on CT
what lobe of the brain is more likely to be the cause of focal epilepsy
temporal
what is radiculopathy
pain in distribution of spinal nerve usually due to compression
most commonly in cervical spine
e.g. sciatica
e.g. spinal stenosis
what causes radiculopathy (9)
degenerative disk disease
osteoarthritis
face joint degeneration
ligament hypertrophy
disk prolapse
spondylolisthesis
radiation
diabetes mellitus
neoplastic disease
how does radiculopathy present and how would you investigate
clinical signs of pain, numbness, weakness
reduced reflexes
spinal MRI of suspected area
nerve conduction studies
BOWSTRING TEST
how is radiculopathy treated
treat underlying cause
what is neurofibromatosis
genetic disorder causes tumours to form on nerve tissue = on brain, spinal cord, nerves
describe type 1 neurofibromatosis
= recklinghausens disease
nerve tissue grows neurofibromas which may be benign
cause damage by compressing nerves and other tissue
describe type 2 neurofibromatosis
bilateral acoustic neuromas develop = hearing loss
how does type 1 neurofibromatosis present (8)
- cafe au lait spots
- freckling = axilla, groin, neck base, sub-mammary
- dermal fibromas = brown nodules on skin, may itch
- nodular neurofibromas = firm clear brown skin growths on trunk may cause parasthesia
- lisch nodules = brown translucent mounds on iris
- short stature
- microcephaly
- nerve root compression
how does type 2 neurofibromatosis present
cafe au lait spots
deafness
vertigo
tinnitus
signs of raising ICP
what are cafe au lait spots
flat light brown patches of skin seen in first year of life
size increase with age
what causes brown-sequard syndorme
intervertebral disc prolapse = most common
MS
tumour
trauma
TB
what is cervical spondylosis
degeneration of annulus fibrosis and osteophyte formation on adjacent vertabra = narrowing of spinal canal and intervetebral foramina
spinal cord dragged over bony spurs and indented when neck flexes and extends = painful
what is carpal tunnel syndrome
inflammation in carpal tunnel = median nerve trapped
most common entrapmetn neuropathy
more women:men
associated with hypothyroidism, DM, pregnancy, RA, acromegaly and obesity
how does carpal tunnel present
pain/parastesia of hand and arm
worse at night, relieved by shaking = SHAKE AND WAKE
loss of sensation in median supplied territories
what investigations are done for carpal tunnel syndrome
phalens test = 1 min maximal wrist flection causes symptoms
tinels test = tapping over nerve at risk = tingling
how is carpal tunnel treated
splinting
steroid injections
decompression surgery
what questionnaires are used in the diagnosis of depression
PHQ-9
GAD-7
what is the sudden loss of vision (like a curtain descending) called?
amaurosis fugax
what is giant cell arteritis and how is it treated
granulomatous arteritis of large vessels
Female, White, over 50, Temporal artery
throbbing headache, tender scalp, jaw claudication
biopsy needed
Tx = prednisolone
what is cushings triad
physiological response to critically high ICP
- hypertension
- bradycardia
- deep/irregular breathing
parkinsons aetiology
lack of dopaminergic neurones in the substantia nigra
associated with lewy bodies
what is significant in prescribing sodium valproate
must NOT be given to female of childbearing age
what is narcolepsy and what is the aetiology
excessive sleepiness due to normal sleep pattern disruption
peptide hypocretin (orexin)
familial link
head trauma/infection/change in sleep habits trigger
= sleep paralysis occurs in 1/3rd
what is cataplexy
sudden loss of voluntary muscle tone triggered by emotion
consciousness is maintained
can ONLY occur with narcolepsy (70% of narcolepsy cases)
slurring speech/double vision/blurred vision can be present
frequency of attacks vary
what investigations are used in narcolepsy/cataplexy
epworth sleepiness scale
sleep studies
EEG
brain MRI to exclude other causes
what is the diagnostic criteria for narcolepsy with cataplexy and without
excessive daytime sleepy >3months
cataplexy symptoms
hypersomnia not better explained by another condition
WITHOUT CATAPLEXY
not present/uncertain episodes
what is the management for narcolepsy
EDS
good sleep hygeine
strategic naps
education and exercise
DRUG
1. modafinil 200mg/day not in pregnancy
2. methylphenidate
3. modafinil + sodium oxybate
others:
SSRI
solriamfetol if modafinil CI
stimulants (amfetamines) but SE
what is the drug treatment for cataplexy
sodium oxybate (GHB)
antidepressents particularly Tricyclic
what is a squint and what are the 2 types
= misalignment of the visual axes
concomitant = common = imbalance in extraocular muscles
paralytic = rare = paralysis of extraocular muscles
how is a squint diagnosed and managed
corneal light reflection test = light 30cm from childs face to see if light refelcts symmetrically
cover test
= refer to secondary care
= eye patches
what is anterior cord syndrome and which tracts are damaged
incomplete spinal cord injury results in infarction of anterior 2/3rds of cord
bilateral spinothalamic and spinocerebellar damage (ascending) = sensory deficits
bilateral corticospinal (descending) = motor deficits
what are the effects of anterior cord syndrome/injury
MOTOR
= sudden onset with PAIN
= motor deficits below level of injury - varies from paraplegia to quadriplegia
SENSORY
= temperature and pain sensation altered 2-3 dermatomes below level of injury
vibration/fine touch/proprioception maintained as tracts are in posterior
what investigation for anterior cord synrome
MRI
= thin pencil-like hyperintensities on sagittal T2
= two bright dots either side of anteiror horn on axial T2
