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Aetiology of Nerve palsies Flashcards

1
Q

what might interupt neural supply

A

Interruption of blood supply
Intracranial vascular abnormality
Space occupying lesion
Ophthalmoplegic migraine
Trauma
Changes in intracranial pressure
Diseases (e.g diabetes, multiple sclerosis)
Inflammatory conditions (e.g meningitis)
Infections
AIDS

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2
Q

what is the prognosis for neurological palsies

A

Recovery more likely:
When treatment of underlying cause successful (Park et al, 2008)

Regression:
Notably in tumours
Spontaneous remission

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3
Q

what can interrupt the blood supply to the nerve

A

Ischaemic attacks (small vascular accidents – due to blockage or bleed)
Isolated palsies in the elderly frequently due to these

Recovery rate - high (e.g 90% of 3rd n palsy by 6/12, Akagi et al, 2008)

Generally stated risk factors:
Diabetes
Arteriosclerosis
Hypertension

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4
Q

What are the different types of vascular accidents

A

Stroke – blood supply to a part of the brain is cut off

Ischaemic Stroke - decreased blood supply caused by a blockage (most strokes)

Haemorrhagic Stroke – bleeding in or around the brain (more rare)

Transient Ischaemic Attack (TIA) - Acute vascular disturbance where the disability lasts less than 24 hours
Infarction - Development 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 platelets, fibrin, clotting factors and cellular elements of blood which become attached to the interior wall of a vein or artery

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5
Q

what are risk factors for the development of 6th nerve palsies and third nerve palsies

A

Patel et al (2005) 6th nerve palsies
Confirmed diabetes as a risk factor – 6 fold increase for diabetes, 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

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6
Q

describe the progression in ishacemic palsies

A

Pain and sudden diplopia typical initial symptoms in ischaemic or compressive disorders

11/16 patients examined within 1 week of onset showed progression (3 to 23 days)

No group differences found, but non-progressive recovered quicker (mean 7.2 weeks c/w mean 11.2 weeks)

Mechanism: ?intraneural compression and further microvascular ischaemia from oedema after initial insult(Jacobson et al, 1995)

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7
Q

how is cocaine linked to oculmotor abnormalities

A

Cocaine abuse should be considered in the differential diagnosis for oculomotor abnormalities especially in the young.
(Nemeth et al, 1993)

Also consider in cases with Myasthenia – may precipitate or exacerbate symptoms

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8
Q

How is giant cell temporal arteritis linked to the development of nerve palsies

A

Inflammatory disease of blood vessels
Affects artery walls, predominantly extracranial vessels - particularly superficial temporal arteries
6% - 70% irreversible visual loss
Occult giant cell arteritis - where there are no systemic symptoms (ocular only)
Median age of onset: 75 years. Rare under 50 years

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9
Q

what is the erythrocyte sedimentation rate in giant cell arteritis

A

Normal: 0-30 mm/hr

Age difference - lower in the young

96% of GCA patients had ESR>50mm/h – hallmark of GCA
(Martinez-Taboada et al, 2000)

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10
Q

what are the systemic signs and symptoms of gca

A

Jaw claudication

Headache

Weight loss

Malaise

Anorexia

Scalp tenderness

Abnormal temporal artery(tender, nodular, or nonpulsating temporal artery)

Myalgia

Fever

Anaemia

Neck pain

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11
Q

what are the ocular findings found in giant cell arteritis

A

symptoms

Amaurosis fugax (painless, transient, monocular or binoc visual loss)
Visual loss
Diplopia
Eye pain

Ocular ischaemic lesions
Anterior ischaemic optic neuropathy (lack of blood supply to ON)
Central retinal vein occlusion
Cilioretinal artery occlusion
Posterior ischaemic optic neuropathy (lack of blood supply to retrobulbar ON)

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12
Q

what are examples of intracranial vascular abnoramlities

A

Aneurysms

Arteriovenous malformations

Fistulas

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13
Q

what are aneuyrsms

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

Symptoms occur from pressure, bleeding or rupture

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14
Q

are aneurysms symptomatic

A

90% asymptomatic until rupture

10% present with mass effect

Interval warning to rupture - 1 day to 4 months (median 14 days) (Barrow and Reisner, 1996)

Rupture: 12% die before receiving medical attention

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15
Q

what are ruptured anyerusms

A

Patients describe 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 & terrible headache needs to be seen as a medical emergency
Aneurysms make leak before they rupture

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16
Q

what ocular involvement occurs in anyerusms

A

Internal carotid and posterior communicating artery 3rd nerve palsy

Intracranial portion of internal carotid Compression anterior visual pathway

Cavernous sinus3rd and 6th nerve Isolated 6th nerve palsy (frequently with ipsilateral Horner syndrome)

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17
Q

what are arteriovenous malformations

A

Congenital, anomalous communications between arterial & venous circulations

Blood is shunted from arteries to veins without an intervening capillary bed

Usually become symptomatic during 2nd & 3rd decades of life

Presence of objective bruit valuable diagnostic sign

Headache - often misdiagnosed as migraine

Signs and symptoms occur due to compression, haemorrhage, ischaemia or vascular steal

18
Q

what are carotid carvenous fistulas

A

Abnormal connection between carotid artery and cavernous sinus

Classified as:
Traumatic or spontaneous
Velocity of flow: High or low
Direct or dural
Internal carotid or external carotid

19
Q

what are the two types of carotid carvenous venous fistulas

A

high flow direct and low flow dural (indirect)

high flow
Often after head injury

Pulsating exophthalmos

Conjunctival chemosis

Cranial Bruit

Diplopia in 60-70%

low flow
Minor signs and symptoms

Onset of redness one or both eyes

Mild proptosis, minimal eyelid swelling, conjunctival chemosis

May or may not be cranial bruit

Diplopia - most often 6th nerve palsy

20-30% result in visual loss

20
Q

what are the characteristics of carvenous sinus syndrome

A

3rd, 4th 6th nerve palsy, alone or in combination (usually ipsilateral)
Oculosympathetic paralysis
Proptosis
Ophthalmic and maxillary division of 5th nerve may be affected
Periorbital or hemicranial pain
Trigeminal neuralgia

21
Q

what is the aetiology of carvenous sinus syndrome

A

Trauma
Vascular (CC fistula, aneurysm, thrombosis)
Tumour (e.g cavernous sinus meningioma)

22
Q

what are types of space occupying lesion

A

Aneurysms

Subdural haematoma

Tumours (Neoplasms)

23
Q

what nerves are affected by what type of tumours

A

4th and sixth nerves most commonly affected

3rd nerve affected in pituitary tumours

Generally suspected where palsy is progressive or does not recover….. but

24
Q

what is a skull base tumour and how is it related to nerve palsies

A

Skull base tumourcan be any type of tumor that forms in the skull base, which is the bottom of the head and the body ridge in the back of the eyes.

25
Q

what is a opthalmoplegic migraine

A

Rare condition – sometimes called intracranial neuralgia
Unilateral headache
Followed by 3rd 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 absence of any pathology

26
Q

how is trauma related to nerve palsies

A

4th nerve particularly susceptible to closed head trauma

6th nerve may be affected if downward displacement of brain stem

3rd nerve least frequently affected by trauma, frontal blow to accelerating head

Shaken baby syndrome – isolated or bilateral palsies may occur

27
Q

what is idiopathic intracranial hypertension

A

Occurs rarely in children
In adults higher incidence in females and in the obese
Main signs and symptoms include:
Headache
Nausea and vomiting
Papilloedema (swelling of optic disc)
Pulsatile tinnitus
6th nerve palsy commonest – 3rd & 4th also reported
Unilateral or bilateral
(NB Also concomitant strabismus or decompensation has been reported)
Can respond to Diamox or gain relief following lumbar puncture

28
Q

when do you get intracranial hypotension

A

Following dural puncture (e.g diagnostic lumbar puncture; accidentally during epidual anaesthesia)

Headache (and nausea), worse when upright, may occur after puncture

Extraocular muscle palsy is a rare complication
6th nerve palsy commonest – 3rd & 4th also reported
Unilateral or bilateral
Onset 1 – 3 days after puncture

(Nishio et al, 2004)
29
Q

how is diabetes related to nerve palsies

A

3rd nerve or 6th nerve most frequently affected

Pupil generally spared

?CauseInterruption of blood supplyInflammation of nerveFocal demyelination

30
Q

why is pupil involvement in a third nerve palsy significant

A

Rule: when aneurysm compresses 3rd nerve, the iris sphincter will be impaired

Do not apply rule where palsy is incomplete

Great caution in the under 50 year age group unless glaring vasculopathic risk factors

31
Q

how does abberent regeneration occur in third nerve palsie

A

Features occur six weeks or more after
onset. Include (alone or in combination):
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 cause

32
Q

what is herpes zoster opthalmicus

A

Virus affects dorsal root ganglia - trigemminal 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 elderly or immuno-compromised

Treated with anti-viral therapy (e.g acyclovir)

33
Q

what is demyleination

A

Multiple SclerosisDemyelination of nerve sheathSuspected in young adults with isolated nerve palsy(most common age for presentation 20 – 40 years; but can be younger or older)

May have other symptoms or history of previous episode
34
Q

what are other inflammatory conditions

A

Meningitis
Encephalitis
Poliomyelitis
Tertiary syphilis (late stage)
Tolosa-Hunt syndrome

35
Q

what is tosola hunt syndrome

A

Non-specific granulomatous inflammation
in anterior part cavernous sinus / SOF area

Possible involvement 3rd, 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)

36
Q

what other diseases are involved in the aetiology of neurological palsies

A

Systemic lupus erythematosus (SLE)
Immunological disorder affecting connective tissue and nervous system
Nerve palsy may be due to vaso-occlusion of small vessels
No cure, pain relief used, if severe immunosuppressives

Sarcoidosis
Granulomatous disease
Isolated or multiple nerve palsies reported, may be accompanied by pain
No cure, but treated with steroids

37
Q

what is Gillian barre syndrome

A

Acute inflammatory demyelinating polyradiculoneuropathy – Aetiology 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 weaks
Ocular involvement to varying extent: ophthlmoplegia, fixed dilated pupils, optic neuritis, facial nerve palsy
Treatment: Intravenous immunoglobulin treatment, steroids, plasma exchange (treatment removes antibodies from blood)

38
Q

what is miller fisher syndrome

A

Possibly a variant of Guillan-Barre
May occur after upper respiratory tract infection
Ophthalmoplegia – usually symmetrical (divergence paralysis, impaired smooth pursuit have also been reported)
Ataxia
Hyporeflexia or areflexia
Diagnosis: Increased protein in CSF from lumbar puncture.
Management: As for Guillan-Barre. Good prognosis.

39
Q

what infections can cause nerve palsies

A

Gradenigo’s Syndrome

Infection of middle ear leading to petrositis and affecting 6th nerve as it crosses petrous part of temporal bone
Ipsilateral pain of trigeminal nerve distribution
Constant ottorhea

40
Q

how is aids related to the cranial nerves

A

Complications may involve cranial nerves:

Infections Parasitic e.g toxoplasmosis Fungal e.g cryptococcosis

Neoplasms

Vascular (high risk of infarct or haemorrhage)

41
Q

what are the causes of multiple cranial nerve palsies

A

Neoplasms
TraumaLess common:
Cavernous Sinus Lesions, Aneurysms, Herpes Zoster, Meningitis, Encephalitis, Tolosa-Hunt, Miller Fisher.

42
Q

what are the causes of congenital neurogenic palsies

A

Congenital conditions
Hydrocephalus
Cerebral palsy
Inherited SO palsy

Intoxications from mother
Lead poisoning, drugs, alcohol

Birth trauma

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