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

Ateiology Of neurological palsies Flashcards

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

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

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

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
Q

what is the ateiology of cavernous sinus syndrome

A
  • trauma
  • vascular ( cc fistula, anyerusm , thrombosis)
  • tumour (e.g. cavernous sinus meningioma)
26
Q

what are examples of space occupying lesions

A
  • anyerusms
  • subdural haematoma
  • tumours (neoplasms)
27
Q

in tumours what cranial nerves are affected

A
  • 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
Q

what is a opthalmoplegic migraine

A

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
Q

what is a neurogenic palsie

A
  • the nervous supply to the
30
Q

describe the relationship between anyerusms and ocular involvement

A
  • 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
Q

in a skull base tumour what nerve palsy is most likely

A

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
Q

what are possible mechanisms for recovery in tumours

A

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
Q

what is a opthalmoplegic migraine

A

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
Q

how are the nerves affected by trauma

A

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
Q

what is idiopthathic intracranial hypertension and what are the signs and symptons

A

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
Q

what is intracranial hypotension

A

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
Q

how is diabetes linked to the ateiology of nerve palsies

A

3rd nerve or 6th nerve is most frequently affected

pupil generally spared

cause - interruption of blood supply , inflammation of nerve

focal demyleination

38
Q

how is the pupil affected in a 3rd nerve palsy

A

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
Q

what is a abberent regenration in relation to a third nerve plasy

A

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
Q

what is herpes zoster opthalmicius

A

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
Q

how is deymyleination related to the ateiology of nerve palsies

A

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
Q

what are other inflammatory conditions that cause neurological palsies

A

meningitis

encephalitis

poilomeyelitis

teritary syphillis

tolosa hunt syndrome

43
Q

what is tosola hunt syndrome

A

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
Q

what other diseases can cause neruological palsies

A

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
Q

how is guilan barrre syndrome related to the ateiology of guillian barre syndrome

A

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
Q

how is miller fisher syndrome related to the ateiology of nerve palsies

A

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
Q

how do infections cause neurological palsies

A
  • 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
Q

how does aids cause neurological palsies

A

compplications may involve cranial nerves

infections - parastic e.g. toxoplasmosis

fungal - cryptoccossis

neoplams

vascular (high risk of infarct or haemmorrhage)

49
Q

what are three top causes of neruolgical palsies

A

incidence of neruological palsies highest- vascular, trauma , neosplasia

50
Q

what are the top 3 causes of neruological palsies

A

neoplasms

trauma

less common

carvenous sinus , lesions , anyerusms, herpes zoster, meningitis , encephalitis , tolosa hunt , miller fisher

51
Q

what has been found in children under 14 year olds in relation to the ateiolgy of 6th neurological palsies

A

neoplasms

trauma
congential

viral

inflmmatory (meningiocephalitis)

idiopathic (3) including bening idioptahtic diagnosis of exclusion

52
Q

what are some causes of congenital neruogenic palsies

A

congneital condiitons

hydrocephalus

cerebral palsy

inherited superior oblique palsy

intoxications from mother - lead posioning , drugs , alchoal ,

birth trauma

53
Q

what are other causes of muscle palsies

A

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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