Ateiology Of neurological palsies Flashcards
what is a neurogenic palsie
- the nervous supply to the muscle is interrupted partially or completley (paralysis)
what may interrupt nerve supply
- interruption of blood supply
- intracranical vascular abnormality
- space occupying lesion
- opthalmoplegic migraine
- trauma e.g. close head trauma - 4th nerve - long course
- change in intracranial pressure - increased intracrnail pressure may press on neural pathways
- disease (e.g. diabetes, multiple sclerosis)
- inflammatroy conditions e.g. meningitis
- infections
- aids
describe the nerve pathway of the third nerve
cn 111 has a superior division and a inferior division
the superior division= the levator palpabrae and the superior rectus
the inferior division = the inferior rectus and the medial rectus and inferior oblique also gives off short cillary and cillary ganglion
what cranial nerve is susceptible to head injuries
cranial nerve 4 travels all the way around the brain so is suceptible to head injuries
what is the prognosis of neurological palsies
recovery is more likely when the treatment of underlying cause is successful (park et al 2008)- ie. if you know what condition has caused the neurogenic palsie - then if you can treat the underlying condition and that treatment is successful then recovery of the nerve palsie is more likely to happen
regression - relapse of symptons
notably in tumours
spontaneous remission- reduction of the signs and symptons of a disease
how is the blood supply to a nerve interrupted and what are the risk factors
ischameic attacks (small vascular accidents due to blockage or bleed) - more common in elderley - transient isachemic attacks - recovery is good
isolated palsies in the elderly freqeuntly due to these
recovery rate high - e.g. akagi 90% of third nerve plasies recover
generally stated risk factors
diabetes
arteriosclerosis
hypertension
age
what are type of vascular accdients
stroke - blood supply to the brain is cut off - can cause neurgenic plasies
ischameic stroke - decreased blood supply caused by a blockage (most strokes)- many of them will have recovery
haemorrhagic stroke - bleeding in or aorund the brain (more rare)
transient isechemic attack - acute ascular dusturbance where the disability lasts less than 24 hrs - may complain of diplopia
infarction - devlopment of an area of localised tissue death (necrosis) as a result of lack of oxygen (anoxia) caused by an interruption in blood supply e.g. occlusion of an artery
thrombosis- aggregation of platlets , fibrin , clotting factors and cellular elements of blood which become attached to the interior wall of a vein or artery
what are risk factors of developing nerve palsies
patel et al 2005 - 6th nerve palsies
confirmed diabetes as a risk factor - 6 fold increase for diabates and 8 fold increase for diabetes and hypertension
hypertension alone - no increase
jacobson et al 1994 - ocular motor nerve palsies
diabetes - 5.75 increase
left ventricular hypertrophy - 5.5. increase not hypertension alone
bascially hypertension alone is not a suffiencet risk factor when coupled with diabetes it is then a risk factor
describe how ischameic palsies progress
- pain and sudden diplopia are typical initial symptons in iscahemic or compressive disorders
- 11/16 patients examined within 1 week of onset showed progression 3-23 days
- no group differences found but non progressive recovered quicker than those that did show increase in their diplopia
- mechanism - intraneural compression and further microvascular ischemia from odema after initial insult
how is cocaine related to neurological palsies
- cocaine abuse should be considred in the differential diagnosis for oculomotor abnormalities, especially in the young - in recently acquired nerugoneic plaises
nemeth et al 1993
also in cases with myasthenia- may percipiate or exaggerate symptons
what is giant cell temporal arterits
temporal artery is in close proximity to the opthalmic artery and the facial artery
- inflammatory disease of blood vessels
- affects artery walls , predominantly extracranial vessels - particulalry superficial temporal arteries
60- 70% irreversible visual loss
occult giant cell arteritis - where there are not systemic symptons (ocular only)
median age of onset - 75 years - rare under 50 years
what is the normal ethrycoyte sedimentation rate in giant cell arteritis
- the erythtocyet sedmentation rate in patients with gca is abnormal
- normal 30- mm / hr
- age difference
- 96% of gca patients had esr > 50mm/h hallmark of gca
what are systemic signs and symptons of gca
- jaw claudication
- headache
- weight loss
- malaise
- anorexia
- scalp tenderness
- abnormal temporal artery (tender , nodular or non pulsating temporal artery
- myaglia
- fever
- anemia
- neck pain
what are ocular findings in gca
symptons = amouris fugax (painless , transient, monocular or binocular visual loss)
visual loss
diplopia
eye pain
what are examples of ocular ischaemic lesions
- anterior ischaemic optic neuropathy (lack of blood supply to on)
- central retinal vein occulsion
- cilioretinal artery occlusion
- posterior iscahemic optic neuropathy (lack of blood supply to retrobulbar ON )
What are examples of intracranial vascular abnormalities
- aneurysms
- arteriovenous malformations
- fistuals
what is a anyerusm
- persistent localised dilations of a blood vessel wall which may result from a developmental defect or be acquired from e.g. acquired degenerative change , infection, inflammation , trauma
symptons occur from pressure , bleeding or rupture
what are the effects patients experience with ayerusms
90 percent are asymptomatic until rupture
10 percent have have an anyerusm with a mass effect
interval waring to rupture 1 day to 4months
12 percent die before recieving medical attention
patients described ruptured anyerusms as the worst headache of their life
medical emergency - aim is to repair the artery and stop bleeding with immediate surgery
any patient presenting with diplopia and terrible headache needs to be seen as a medical emergency
anyerms make leak before they rupture
what is a arteriovenous malformation
congenital anomolous communications between arterial and venous circulations
blood = shunted from arteries to veins without an intervening capillary bed
usually become symptomatic during second and third decades of life
presence of objective bruit valuable diagnositc sign
headache - often misdiagnosed as a migraine
signs and symptons occur due to compression haemorrhage, ischaemia or vascular steal
what is a cartotid carvenous fistulus
- abnormal connection between carotid artery and cavernous sinus
what are the different classifications of carotid carvenous fistulas
classified as
- traumatic or spontaneous
velocity of flow= high or low
direct or dural
internal carotid or external carotid
what are the signs of a high flow caotid carvernous sinus fistula
- often after head injury
- pulsating exopthalmos - when the eye is bulging forwards and pulsating
- conjuctival chemosis
cranial bruit - you will hear blood going through vessel
diplopia in 60-70%
what are the signs of a low flow cavernous sinus fistula
minor signs and symptons
onset of redness one or both eyes
mild proptosis , minimal eyelid swelling , conjuctival chemoisis
may or may not be cranial- bruit - (audible vascular sound associated with turbulent blood flow)
diplopia- most often 6th nerve palsy
20-30% result in visual loss
what are the characterisitcs of cavernous sinus syndrome
- 3rd , 4th nerve , 6th nerve palsy , alone or in combination (usually ipsilateral)
- oculosympathetic parylis
- proptosis
- opthalmic and maxillary division of 5th nerve may be affected
- preorbital or hemicranial pain
trigeminal neraglia
what is the ateiology of cavernous sinus syndrome
- trauma
- vascular ( cc fistula, anyerusm , thrombosis)
- tumour (e.g. cavernous sinus meningioma)
what are examples of space occupying lesions
- anyerusms
- subdural haematoma
- tumours (neoplasms)
in tumours what cranial nerves are affected
- 4th and 6th nerves are most commonly affected
- 3rd nerve affected in pituitary tumours
- generally suspected where palsy is progressive or does not recover
what is a opthalmoplegic migraine
rare condition - sometimes called intracranial neuralgia
unilateral headache
followed by a third nerve palsy - partial or complete , pupil often affected
6th nerve may be affected and a suggested cause of recurrent 6th nerve palsy in children in the absence of any pathology
what is a neurogenic palsie
- the nervous supply to the
describe the relationship between anyerusms and ocular involvement
- internal carotid and posterior communicating artery
3rd nerve palsy
-intracranial portion of internal carotid
compression anterior visual pathway
- carvernous sinus
3rd and 6th nerve
isolated 6th nerve palsy (frequently with ipsilateral horner syndrome)
in a skull base tumour what nerve palsy is most likely
a remitting sixth nerve palsy has been found in skull base tumouts
7 cases reported recovery 1 week to 18 months
all patients recovered at least once and did so without chemotherapy surgical intervention or radiotherapy
volpe and leseel 19937
what are possible mechanisms for recovery in tumours
possible mechanisms for recovery include remyleination axonal regernation relief of transient compression , retoration of impaired blood flow slippage of a nerve previously stretched over tumour, immune responses to a tumour
what is a opthalmoplegic migraine
rare condition sometimes called intracranial neruaglia
unilateral headache
followed by 3rd nerve palsy partial or complete, pupil often affected
6th nerve may be affected and a suggested cause of a recurerent 6th nerve palsy in children in the absence of any pathology
how are the nerves affected by trauma
4th nerve is the most susceptible to closed head trauma
6th nerve may be affected if downward displacment of the brain stem
3rd nerve least freqeuntly affected by trauama , frontal blow to acceleratig head
shaken baby syndrome - isolated or bilateral palsies may occur
what is idiopthathic intracranial hypertension and what are the signs and symptons
occurs rarely in children
in adults higher incidence in females and in the obese
main signs =
headache , nausea and vomiting, papioldemea (swelling of the optic disc)
pulsatile tinnitus- ear
6th nerve palsy commonest
unilateral or bilateral
also be shown to occur in concommitant deviations and decompensation
Can respond to diamox or gain relief following a lumbar puncture
what is intracranial hypotension
following dural puncture (e.g. diagnostic lumbar puncture , acidentally during epidual anaesthesia
headache and nausea - worse when upright - may occur after puncture
eom muscle palsy is a rare complication
- 6th nerve plasy commonest - 3rd and 4th also reported
unilateral or bilateral
onset 1-3 days after puncture
nishio et al 2004
how is diabetes linked to the ateiology of nerve palsies
3rd nerve or 6th nerve is most frequently affected
pupil generally spared
cause - interruption of blood supply , inflammation of nerve
focal demyleination
how is the pupil affected in a 3rd nerve palsy
when anyerusm compresses 3rd nerve the iris sphincter will be impaired
do not apply rule where palsy is incomplete - applies when they have a ptosis
great caution in under 50 year age group unless glaring vascilopathic risk factors
what is a abberent regenration in relation to a third nerve plasy
features occur six weeks or more after onset
- after the eye and the nerve starts to refunction - you begin to get recovery of the function
symptons include
retraction of upper lid on down gaze
elevation of upper lid on adduction
constriction of the pupil on elevation , depression or adduction
adduction on attempted elevation (and occasionally on depression)
tends to occur where trauma or space occupying lesion is the cause
what is herpes zoster opthalmicius
virus affects dorsal root ganglia - trigeminal ganglia affected - unilateral painful rash
muscle palsies may be ipsilateral, contralateral or bilateral and may affect one or more nerves
can affect any age , but more common in elerley or immuno- comprimised
treated with anti- viral therapy ( e.g. acylovir)
how is deymyleination related to the ateiology of nerve palsies
multiple sclerosis
demyelination of nerve sheath
suspectef in young adults with isolated nerve palsy
most common age for presentation 20-40 years but can be younger or older
may have other symptons or history of previous episode
what are other inflammatory conditions that cause neurological palsies
meningitis
encephalitis
poilomeyelitis
teritary syphillis
tolosa hunt syndrome
what is tosola hunt syndrome
non specific granulomatous inflammation in anterior part carvenous sinus / sof area
possible involvement 3rf, 4th, 6th nerves with severe constant pain
visual loss if on involved
proptosis
sluggish pupil
diagnosis ; ct scan , esr may be raised
treatment : systemic steroids e..g prednisolone
what other diseases can cause neruological palsies
systemic lupus erythematosus (sle)
immunolgical disorder affecting connective tissue and nervous tissue
nerve palsy may be due to vaso- occlusion of small vessels
no cure, pain relief used, if severe immunosupressives
sarcodosis
granulmoatosus disease - isolated or multiple nerve palsies reported may be accompanied by pain
no cure but treated with steroids
how is guilan barrre syndrome related to the ateiology of guillian barre syndrome
acute inflammatory demyelinating - ateiology not fully understood - may occur after viral infection
slightly more common in males than females , can affect any age , but most common 20-50 yrs age
sudden acute motor paresis peaking within 4 weeks
ocular involvement to varying extent opthalmalegia, fixed dilated pupils , optic neuritis , facial nerve palsy
treatment intravenous immunoglobin treatment , steroids plasma exchange (treatment removes antibodies from blood)
how is miller fisher syndrome related to the ateiology of nerve palsies
possibly a variant of guillian barre
may occur after upper respiratory tract infection
opthalmlopegia- usually symmetrical divergence paralysis , impaired smooth pursuit have also been reported
ataxia
hyporeflexia or areflexia
diagnosis: increased protein in csf from lumbar puncture
management; good prognosis
how do infections cause neurological palsies
- gradenigios syndrome - inection of middle ear leading to petrosis and affecting 6th nerve as it crossed petrous part of temporal bone
- ipsilateral pain of trigeminal nerve distribution
constant ottorhea
how does aids cause neurological palsies
compplications may involve cranial nerves
infections - parastic e.g. toxoplasmosis
fungal - cryptoccossis
neoplams
vascular (high risk of infarct or haemmorrhage)
what are three top causes of neruolgical palsies
incidence of neruological palsies highest- vascular, trauma , neosplasia
what are the top 3 causes of neruological palsies
neoplasms
trauma
less common
carvenous sinus , lesions , anyerusms, herpes zoster, meningitis , encephalitis , tolosa hunt , miller fisher
what has been found in children under 14 year olds in relation to the ateiolgy of 6th neurological palsies
neoplasms
trauma
congential
viral
inflmmatory (meningiocephalitis)
idiopathic (3) including bening idioptahtic diagnosis of exclusion
what are some causes of congenital neruogenic palsies
congneital condiitons
hydrocephalus
cerebral palsy
inherited superior oblique palsy
intoxications from mother - lead posioning , drugs , alchoal ,
birth trauma
what are other causes of muscle palsies
nucleus - aplasia , hypoplasia , maldevelopment
nerve - as above or incorrect distribution
muscle - aplasia: abnormal insertion check ligamaents or connections
orbit- malformation
