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212- S + OM > Ateiology Of neurological palsies > Flashcards

Ateiology Of neurological palsies Flashcards

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1
Q

what is a neurogenic palsie

A
  • the nervous supply to the muscle is interrupted partially or completley (paralysis)
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2
Q

what may interrupt nerve supply

A
  • 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
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3
Q

describe the nerve pathway of the third nerve

A

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

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4
Q

what cranial nerve is susceptible to head injuries

A

cranial nerve 4 travels all the way around the brain so is suceptible to head injuries

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5
Q

what is the prognosis of neurological palsies

A

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

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6
Q

how is the blood supply to a nerve interrupted and what are the risk factors

A

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

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7
Q

what are type of vascular accdients

A

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

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8
Q

what are risk factors of developing nerve palsies

A

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

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9
Q

describe how ischameic palsies progress

A
  • 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
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10
Q

how is cocaine related to neurological palsies

A
  • 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

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11
Q

what is giant cell temporal arterits

A

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

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12
Q

what is the normal ethrycoyte sedimentation rate in giant cell arteritis

A
  • 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
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13
Q

what are systemic signs and symptons of gca

A
  • jaw claudication
  • headache
  • weight loss
  • malaise
  • anorexia
  • scalp tenderness
  • abnormal temporal artery (tender , nodular or non pulsating temporal artery
  • myaglia
  • fever
  • anemia
  • neck pain
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14
Q

what are ocular findings in gca

A

symptons = amouris fugax (painless , transient, monocular or binocular visual loss)

visual loss

diplopia

eye pain

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15
Q

what are examples of ocular ischaemic lesions

A
  • 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 )
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16
Q

What are examples of intracranial vascular abnormalities

A
  • aneurysms
  • arteriovenous malformations
  • fistuals
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17
Q

what is a anyerusm

A
  • 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

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18
Q

what are the effects patients experience with ayerusms

A

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

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19
Q

what is a arteriovenous malformation

A

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

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20
Q

what is a cartotid carvenous fistulus

A
  • abnormal connection between carotid artery and cavernous sinus
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21
Q

what are the different classifications of carotid carvenous fistulas

A

classified as

  • traumatic or spontaneous

velocity of flow= high or low

direct or dural

internal carotid or external carotid

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22
Q

what are the signs of a high flow caotid carvernous sinus fistula

Study These Flashcards
A
  • 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%

23
Q

what are the signs of a low flow cavernous sinus fistula

Study These Flashcards
A

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

24
Q

what are the characterisitcs of cavernous sinus syndrome

Study These Flashcards
A
  • 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

25
what is the ateiology of cavernous sinus syndrome
- trauma - vascular ( cc fistula, anyerusm , thrombosis) - tumour (e.g. cavernous sinus meningioma)
26
what are examples of space occupying lesions
- anyerusms - subdural haematoma - tumours (neoplasms)
27
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
28
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
29
what is a neurogenic palsie
- the nervous supply to the
30
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)
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
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
40
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)
41
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
42
what are other inflammatory conditions that cause neurological palsies
meningitis encephalitis poilomeyelitis teritary syphillis tolosa hunt syndrome
43
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
44
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
45
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)
46
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
47
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
48
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)
49
what are three top causes of neruolgical palsies
incidence of neruological palsies highest- vascular, trauma , neosplasia
50
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
51
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
52
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
53
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

212- S + OM (10 decks)

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