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Cranial nerves Flashcards

1
Q

how many Extraocular muscles are there ?

What nerves are the innervated by ?

A

7

  • superior oblique
  • inferior oblique
  • Superior rectus
  • Inferior rectus
  • lateral rectus
  • medial rectus
  • lateral palpebrae
    superioris
  • Rectus and oblique muscles responsible for eye movements
  • levator palpebrae superioris - responsible for superior eye lid movements
     - oculormotor nerve  0 has both voluntary and involuntary control of eye movement .
  • Latin - means elevator of the upper eye lid.
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2
Q

What types of eye movement can the be done ?

A
  • Elevation - up
  • Depression - down
  • adduction - medial movement
  • abduction - lateral movement
  • intorsion - internal rotation - towards nose
  • extorsion - external rotation - way from nose
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3
Q

Eye movement - superior rectus ?

innervation

A

elevation
adduction - medial movement
Intorsion

oculomotor nerve

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4
Q

Eye movement - inferior rectus ?

innervation

A

depression
adduction - medial
extorsion - lateral rotation

oculomotor nerve

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5
Q

Eye movement - medial rectus ?

innervation

A

Adduction - medial movements

oculomotor nerve - 3

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6
Q

Eye movement - lateral rectus ?

innervation

A

Abduction

Abducens - 6

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7
Q

Eye movement - superior oblique ?

innervation

A

depression
abduction
intorsion

Trochlea -4

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8
Q

Eye movement -inferior oblique ?

innervation

A

elevation
abduction -medial
extorsion - lateral rotation

oculomotor nerve

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9
Q

Note * muscles work in coordinated manner to produce eye movement

A

ex. Elevation produced by both superior rectus and inferior oblique
- However , superior rectus involved in adduction , inferior oblique involved in abduction

so when eye is abducted - inferior oblique dominantly responsible

when adducted - superior rectus dominantly responsible

similar principle with depression involving inferior rectus and superior oblique

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10
Q

What is oculomotor nerve palsy ?

A

Eye condition - causes impaired eye movements

Presentation

0 Affected eye - moves outwards and downwards.
* affected eye can turn on move to the middle when looking inwards. CANNOT MOVE UP AND DOWN.

0 eye lid droop

0 dilated pupil (may not constrict in response to light) - pupil usually affected when palsy cause by compression.

0 Unaffected eye looks straight

  * causes double vision

Causes

  • Compression - Aneurysm , herniation
  • inadequate blood flow -
  • life threating - if condition causing palsy worsens, Can lead to deep coma and possible brain death - indicated by both pupils dilated and no response to light.
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11
Q

Diagnosis of oculomotor nerve palsy ?

A
  • neurological examination - diagnosis of palsy
  • MRI or CT scan - done to identify cause of palsy
    * if no blood detected then one of these are done :
    0 spinal tap/ lumbar puncture,
    0 CT angiography
    0 Magnetic resonance angiography
    0 cerebral angiography
  • you choose which one.
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12
Q

What is trochlea nerve palsy ?

A

eye condition of the 4th cranial nerve

effects vertical movements - trochlea nerve supplies superior oblique involved in depression of eye.

Person will tilt head in direction opposite to affected side to eliminate double images.

Causes

  • head injury (motorcycle - accident - is common ) -MOST COMMON
  • diabetes - damage small blood vessels that carry blood to the nerve -

rare - tumor , aneurysm , multiple sclerosis

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13
Q

Diagnosis of Trochlear nerve palsy ?

A
  • limited eye movements

- MRI or CT scan - done to identify cause

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14
Q

Treatment of trochlear nerve palsy ?

A
  • treatment of underlying cause
  • eye exercises
  • prism glasses - bend light to adjust for double vision
  • usually resolves over time - however sometimes surgery is needed ?
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15
Q

Symptoms , cause of MS ?

A

Demyelination - Autoimmune - immune system attacks and destroys myelin and underlying nerve fibres—————> slows down conduction & cause neuroinflammation & degeneration.

Pseudobulbar /upper neurone pattern of weakness - will cause reduced gag reflex and emotional lability.

  • cause not actually known - but autoimmune may be involved.

Patients have periods of good health (remissions) followed by worsening symptoms(relapses) , MS gets worse over time.

Symptoms vary greatly - depends which nerves are demyelinated.

  • vision problems
    • internuclear ophthalmoplegia -impairment of horizontal eye movements - damage to CN3,4,6.
    • optic neuritis - inflammation of optic nerve.
  • abnormal sensations - demyelination of sensory neurones
    e.g.
    o parathesia - tingling sensation
    o pain
    o Hypoesthesias - reduced sensation
  • movements weak and clumsy - demyelination of motor neurones.
    e. g ;
  • Spasms
  • Ataxia
  • Weakness
  • dizziness and vertigo , fatigue
  • Lhermitte sign - electric shock , tingling sensation that shoots down back , down both legs , down one arm or one side of the body.
    • last moment and disappears when back straightened.
      Normally , felt as long as neck is bent.

other ones - just for knowlegde

o MS Hug - tight band like sensation around body - due to spinal cord lesion

o Uhthoff Phenomenon - temporary worsening of MS symptoms due to increase in temp - body get overheated in hot weather , baths , saunas etc.

( differs from motor neurone disease - mnd does not cause sensory loss )

RISK FACTORS
- More common in women
-

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16
Q

What are the patterns of MS ?

A

0 relapsing - remitting patterns - relapses followed by remissions - cycle
- happens because myelin recover & regenerate (remitting) but then happens again (relaspe)

0 primary progressive - no remissions or obvious relapses - it just gets worse
*can have temporary plateaus - where it does not get worse but does not get better.

0 Secondary progressive pattern - starts off as relapsing - remitting but then progressively gets worse.
(scarring is taking place - less regeneration occuring. )

0 progressive relapsing pattern - progresses gradually , but progression is interrupted by sudden relapses - rare.

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17
Q

What is internuclear Ophthalmoplegias ?

A

Impaired horizontal eye movements - damage to CN3,4,6

One eye cannot turn inwards - double vision when looking direction of unaffected eye

Nystagmus - unaffcted eye rapidly moves from side to side

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18
Q

Later symptoms of MS ?

A

Symptoms of MS due to central lesion in brain / spinal cord

Slow /slurred speech

depression

Cannot laugh or cry appropriately

Uninary problems 
       - urinary retention - 
         increase risk of UTI
       - urinary incontinence 
       - difficulty urinating 
       - frequent / strong urges 
         to urinate

Constipation
occasional fecal incontinence.

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19
Q

Diagnosis of MS

A

0 comprehensive history

0 Brain MRI - most common
(can show lesions perpendicular to lateral ventricles
-Calloso-septal interface ( inferior surface of the corpus callosum, where the septum pellucidum abuts it. )
- Barinstem e.g pons
- 95 % of patients have a positive MRI
0 spinal cord MRI
(should show demyelinated lesions -short lesions (less than 2 segments)

All of these should be normal, done to rule out other conditions.
- FBC - should be normal in MS

  • Comprehensive metabolic panel -
  • TSH - Thyroid stim hormone -
  • Vitamin B12

INVESTIGATIONS TO CONSIDER

0 CSF fluid sample
- presence of oligoclonal bands - only in csf not serum . If in serum and csf indiate systemic illness not only CNS.
- elevated IgG and IgG synthesis rates
(these present in 80 of MS cases)

0 Anti-neuromyelitis optica antibody testing - present in Devic syndrome

  • in patient with long segment of spinal cord demyelination + / - optic neuritis (ON) or normal brain inaging with ON

0 neurological exam

0 ophthalmoscope - optic disc may be usually pale indicating optic nerve damage.

0 MRI - detect areas of demyelination

* Gadolinium contrast added to blood stream after first MRI detects demyelination. MRI done again  - Gadolinium - distinguish btw recent areas or long standing areas of demyelination. (stable to progressive)

Doctor mays may suspect MS in young people who present with sudden blurred vision , double vision , movement problems , abnormal sensations in unrelated parts of the body.

*pattern of relapses and remissions supports this.

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20
Q

Treatment of MS

A

ACUTE
1ST LINE
Corticosteroids - e.g. IV Methylprednisolone - (mostly high dose , IV , if not can be given orally)

treatment started and stopped when needed not long term because of side effects.

  • control symptoms

ADJUNCT
Plasma exchange -
(in patients with severe or rapidly progressing disability. )

RELASPING - REMITTING PATTERN

1st line
Immunomodulators e.g.:
- interferon beta
- glatiramer,
- dimethyl fumarate,
- teriflunomide(tetragenic - not used in men/womeh trying to concieve children)
these used most often
- ocrelizumab
- natalizumab etc.
secondary options
Alemtuzumab - not used in:
- certain heart , circulation & bleeding disorders.
- on signs of stroke , tears in arteries in head and neck - consider stopping.
- ACTIVE MONITORING HOSPITAL WITH THIS DRUG.
Fingolimod - tertiary option - contraindicated in pre - existing cardiac disease - can cause bradycardia

FATIGUE

  • physical activity
  • relaxation
  • ADJUNCT - amantadine , modafinil , armodafinil - fatigue does not stop.

URINARY FREQUENCY

  • Medication e.g oxybutin
  • self catherisation

INCREASED MUSCLE TONE + /- spasm
Physiotherapy + antispasticity medications

  • Gentle stretching
  • Baclofen- muscle relaxant - controls spascity
  • Clonazepam

TREMOR

  • Propranolol
  • Primidone
  • Clonazepam
SENSORY SYMPTOMS
(low dose anticonvulsants )
- Gabapentin
- Pregabalin
- Carbamazepine

GAIT problems
- Physio + / or PRT - progressive resistance training.

SECONDARY PROGRESSIVE
1ST LINE
Siponimod or methylprednisolone

2ND LINE
Cladribine

PRIMARY PROGRESSIVE
- Ocrelizumab

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21
Q

What are the sensory branches of the trigeminal nerve (5)

A

V1 - ophthalmic
V2 - maxillary
V3 - mandibular

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22
Q

Which nerve innervates parotid gland ?

A

glossopharyngeal - 9

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23
Q

Function of Accessory nerve ?

A

motor innervation of trapezius ad sternocleidomastoid muscle.

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24
Q

Function of Hypoglosaal nerve ?

A

Innervates tongue.

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25
Q

Pathway of optic nerve ?

A

Retina —–> travel through optic disc ——> optic chiasm ——- > optic tract ——>lateral geniculate nuclei —–> visual cortex

Optic nerves from medial side of retina (closes to nose )cross over

Optic nerves from lateral retina don’t cross over

26
Q

Optic nerve damage ?

A

Damage

  • before optic chiasm - affect both nasal and temporal visual fields.
    e. g damage to left side —-> left eye blind
  • at optic chiasm - bitemporal heminopia
  • After chiasm - homonymous heminopia
  • one of tract effected (after chiasm ) - homonymous superior quadrantanopia
27
Q

Optic nerve pathway -what supplies what.

A

left lateral fibre (that does not cross over at chiasm ) - supplies left nasal field (near nose)

*carry info to left geniculate nuclei where it synapses with nerve that carries Info to occipital lobe -visual cortex

Right medial (near nose) fibre - capture images from right temporal field

  • cross over at chiasm - carry info to left geniculate nuclei where it synapses with nerve that carries Info to occipital lobe -visual cortex

SAME PRINCIPLE FOR RIGHT JUST REPLACE LEFT WITH RIGHT

medial fibre = temporal visual field
lateral fibre = nasal visual field

MTLN - Mummy Took Laurenda’s Name

28
Q

Complications to vision when macula damaged ?

A

Macula - contain fovea - pigmented cells - cone cells - needed for central vision.

Central scomata - macular degeneration - loss of central vision.

Constricted visual fields - damage to everything but macula
* seen Glaucoma and retina pigmentosa

Glaucoma - eye condition - build up of fluid and increasing pressure.

retina pigmentosa - group of inherited vision disorders that cause progressive degeneration of the retina - peripheral vsion decreases - central vision usually preserved until late stages.

29
Q

Treatment of Glaucoma ?

A

medicine to reduce pressure in the eye :

Eyedrops

  • Topical prostaglandins
    0 Latanoprost
    0 travoprost
    0 Tafluprost
  • Miotics - Pilocarpine hydrochloride.

(*help drain fluid from eye )

  • Beta blockers
    0 Betaxolol
    0 levobunolol
    0 Timolol

(* lowering amount of fluid the eye makes)

Carbonic anhydrase  inhibitors - 
     0brinzolamide -topical
0 Dorzolamide 
  - topical
0 oral + parenteral  Acetazolamide (oral - not recommended for long term use)
  • Alpha-adrenergic agonists -sympathomimetic agents
    0 Brimonidine tartrate (typically used when beta blocker is inappropriate )
    0 Apraclonidine
30
Q

Pituitary adenoma and optic nerve ?

A

enlargement of gland can compress optic chiasm - lies in close proximity - can cause bitemporal heminopia

31
Q

What is retinal detachment ?

A

Retina become loose - pulls away from BV.

Can be caused by retinal tear

Characterised BY :

0 Flashes of light in one or both eyes (photopsia)

0 The sudden appearance of many floaters — tiny specks that seem to drift through your field of vision

0 Darkness or a “curtain” over your vision, including the middle or the sides

  • Needs to be treated quickly to prevent permanent damage to eye
    sight.

The most common location for a retinal tear is in the supratemporal quadrant (60%)

32
Q

What is Vitreous haemorrhage ?

A

Visual impairment

Mostly effects one eye.

Blood leaks into vitreous humour (fluid at back of eye - needs to clear for light to pass through it to reach retina)

0 painless unilateral floaters and/or visual loss.

floaters,

cobwebs,

haze,

shadows

red hue

33
Q

central retinal artery occlusion

A

Blockage of this artery - supplies retina

Loss of eyesight in the affected eye .

If blood clot breaks free can
go to brain cause stroke.

34
Q

Central retinal vein occlusion

A

blockage of this vein - leakage of blood and excess fluid into the retina.

fluid can collects macula - responsible for central vision - cause blurry central vision

35
Q

What is Guillain Barre syndrome ?

Triggers
Types
Investigations

A

Auto - immune condition - immune system attacks nerves and damages them.

Two-thirds of patients have a history of gastroenteritis or influenza-like illness weeks before onset of neurological symptoms.(some sort of infection)

Triggers

0 infection - can happen a few days or weeks after infection,

vaccination - more rare - but increased risk.

surgery

Infection is the most common cause.

2types
0 Axonal or demyelinating

Main Investigation 
0 Nerve conduction studies
0 Lumbar puncture - raised CSF protein -
0 LFTs - raised AST/ALT
0 Spirametry - 6 hour intervals at bedside.
36
Q

Symptoms of Guillain - Barre Syndrome ?

A

Usually develop over hours or days and tend to start in your feet and hands before spreading to your arms and legs.

At first you may have:

numbness
pins and needles
muscle weakness - usally affects lower extremities before upper. (opposite of botulism)
pain
problems with balance and co-ordination
These symptoms usually affect both sides of the body at the same time.

Later symptoms
The symptoms may continue to get worse over the next few days or weeks.

Some people are only mildly affected, but others may have:

  • mild sensory symptoms on exmaination - if so unlikely to GBS.
    (Paraesthesia) in hands & feet (80% of pl -from top to bottom -procedes weakness often)

0 difficulty walking without assistance

0 an inability to move the legs, arms and/or face (paralysis)

0 reduced / absent reflexes

0 facial weakness - BILATERAL (often)

0 difficulty breathing - 30% of pl with develop respiratory muscle weakness (require muscle ventilation).

0 blurred or double vision

BULBAR DYSFUNCTION CAUSING OROPHARYNGEAL WEAKNESS.

0 difficulty speaking (slurred speech)
problems swallowing or chewing

0 difficulty peeing, and constipation
persistent and/or severe pain

0 dysautonomia - automic system noot working properly etc (autonomic dysfunction)

0 back / leg pain - can be mistaken for spinal cord compression.

Guillain-Barré syndrome usually reaches its most severe point within 4 weeks, remain stable for a few weeks or months before gradually improving.

37
Q

Treatment of Guillan Barre syndrome ?

A

0 intravenous immunoglobulin (IVIG ) - most commonly used .

donated blood contains healthy antibodies which help stop harmful antibodies damaging nerves.

0 Plasma exchange (Plasmapheresis )

attached to machine - removes blood from vein filtering out harmful antibodies.

treatment over 5 days.

38
Q

Treatment of Myasthenia Gravis ?

A

0 Pridostigimine - 1st line - Tablet - helps electrical signals travel between nerves and muscles.

Acetylcholinesterase inhibitor - prevents breakdown of ACH.

last a few hours - multiple needed a day.

Steriods e.g prednisolone - if Pyridostigmine does not work or provides ony short term relief.

Imunnospressant - if neither work or steriod dose is high (unpleasant side effects ) - azathroprine or mycophenolate.

0 Need to arrange CT upper scan - thymic hyperplasia seen in younger women with MG and older patients are predisposed to thymomas (thymic tumor )

39
Q

What should you warn patient of after diagnosis of MG ?

A

Myasthenic crisis can be triggered by:

  • certain drugs
  • sudden medication discontinuation.
  • neuromuscular blocking agents used in anaesthesia.

advise to wear med - alert bracelet ( alert staff to condition)

40
Q

What is the meaning if clinically isolated syndrome .

A

CIS is a first episode of neurologic symptoms caused by inflammation anddemyelinationin the central nervous system.

must last for at least 24 hours

characteristic of multiple sclerosis but does not yet meet the criteria for adiagnosis of MSbecause people who experience a CIS may or may not go on to develop MS.

CIS is accompanied by lesions on a brain MRI similar to those seen in MS, - high likelihood of a second episode of neurologic symptoms and diagnosis of relapsing-remitting MS.

When CIS is not accompanied by MS-like lesions on a brain MRI, the person has a much lower likelihood of developing MS.

41
Q

What is myasthenia crisis ?

A

Life threatening complication of MG. Patients breathing / respiratory muscles get so weak and stop working
So cannot breathe.

Require incubation.

Th

is is not the same as a myasthenia gravis flare up.

Patient with MG symptoms worsen.

42
Q

What is myasthenia gravis ? Symptoms

A

Rare long term condition - causes muscle weakness

Autoimmune condition - auto antibodies block acetylcholine receptors at neuromuscular junction so block in transmission —————-》 muscle does not contract

Sometimes can be linked to thymus gland ( regulates immune system) ——》 usually get smaller /replaced by fat ——– in some cases it is not ———- remains large / tumours can form
‐——-》 gives incorrect instructions to immune cells.
.

Typically starts in women aged 40 and over and in men 60 and over.

Symptoms

droopy eyelids

double vision

difficulty making facial expressions

problems chewing anddifficulty swallowing

slurred speech

weak arms, legs or neck

shortness of breathand occasionally serious breathing difficulties

Symptoms tend to be worse when tired - so before bed and better when u wake up from sleep.

43
Q

What muscle/ nerve is being used when eye is being elevated & abducted )

A

Superior rectus only

Oculomotor nerve - CN 3

44
Q

What muscle/ nerve is being used when eye is being depressed & abducted )

A

Inferior rectus only

Oculomotor nerve

45
Q

What muscle/ nerve is being used when eye is being elevated & adducted )

A

Inferior oblique only

Oculomotor nerve

46
Q

What muscle/ nerve is being used when eye is being depressed & adducted )

A

superior oblique only

Trochlear nerve

47
Q

How do you isolate the actions of the muscles involved in depression?

A

The responsible muscle varies depending on whether the eye is abducted or adducted
Note how superior oblique can pull its insertion two ways due to its insertion relative to the axes of the eye:
To intort and depress (down and out)

Note how inferior rectus can pull in two ways:
to extort and depress (down and in)

If we abduct the eyeball we can see that inferior rectus depresses and superior oblique intorts.

If we adduct the eyeball superior oblique depresses and inferior rectus extorts

48
Q

Diagnosis of myasthenia gravis

A

Anyi - MuSK antibody & acetylchokine receptor antibodies - elevated ( sometimes not present —i.e. in ocular myasthenia gravis - only effects extraordinary muscle - causes weakness - double vision , dropping eyelids)

An edrophonium test. This test uses injections of edrophonium chloride to briefly relieve weakness in people with myasthenia gravis. The drug blocks the breakdown of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. It is usually used to test ocular muscle weakness.

( rarely done because of side effects nowdays - only if it is really needed)

Mri or CT - detect possible thyoma

49
Q

CSF protein levels- what do levels indicate?

Lumbar puncture used to test CSF fluid

A

CSF protein concentration may rise due to 2 factors: either an increased permeability of the blood brain barrier allowing more protein and higher molecular weight proteins to enter the CSF or proteins may be synthesised within the cerebrospinal canal by inflammatory or other invading cells.

Mild protein elevation may be caused by viral meningitis, neurosyphilis, subdural haematoma, cerebral thrombosis, brain tumour, multiple sclerosis (rarely >1.00 g/L)

Moderate or pronounced elevation may be caused by acute bacterial meningitis, tuberculous meningitis, spinal cord tumour, cerebral haemorrhage, Guillain-Barre syndrome.

50
Q

What is hornet’s syndrome?

A

Horner syndrome is a relatively rare disorder characterized by :

O a constricted pupil (miosis),

O drooping of the upper eyelid (ptosis),

Oabsence of sweating of the face (anhidrosis),

O sinking of the eyeball into the bony cavity that protects the eye (enophthalmos)
These are the four classic signs of the disorder

CAUSES

o carotid artery dissection

o tumor is neck or chest
- pancoast tumor - in upper part if lung

o lesions in neck , brainstem ,upper spinal cord or eye orbit.

Lesion/ tumor usually found on the path to the eye- disrupting sympathetic innervation.

51
Q

What is inclusion body myositis?i

A

Inclusion body myositis (IBM)

is a progressive muscle disorder characterized by muscle inflammation, weakness, and atrophy (wasting). It is a type ofinflammatory myopathy. IBM develops in adulthood, usually after age 50. The symptoms and rate of progression vary from person to person.

common symptoms include progressive weakness of :

O legs, arms, fingers, and wrists.

O Some people also have weakness of the facial muscles (especially muscles controlling eye closure),

O difficulty swallowing (dysphagia).

Muscle cramping and pain are uncommon, but have been reported in some people.[1][

Mimics MND - motor neurone disease

Complications

Aspiration pneumonia - aspiration of food , salvia leads to infection /inflammation of the lungs.

52
Q

What is Multiple sclerosis ?

A

Multiple - multiple lesions

Sclerosis - scarring
Affects predominately white mater.

Autoimmune demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of CNS .e.g:
o brain
o spinal cord,
o optic nerves) separated in time and space
( they happen at different times )
- different dates , different places.

Most commonly diagnosed from 20 -40

KEY DIAGNOSTIC FACTORS

0 Visual disturbance in one eye e.g
- Blurred vision
- pain on eye movement
(effects white mater of brain so can effect optic nerve - made of similar material - cause optic neuritis)
- loss of colour peception
- Intranuclear opthlamapegias - optic neuritis

0 abnormal senssations
- Lhermitte’s sign , MS banding etc.

RISK FACTORS

  • Female
  • more common in white females

WEAK
- EBC virus - epstein barr - higher risk of MS development

  • History of autoimmune disease
  • Vitamin D deficiency
  • Smoking
53
Q

What is Devic syndrome?

A

Neuromyelitis optica spectrum disorder (NMOSD), also known as Devic disease, is a chronic disorder of the brain and spinal cord dominated by inflammation of the optic nerve (optic neuritis) and inflammation of the spinal cord (myelitis).

  • normally one episode with no reoccurrence - lasting says or weeks

early stages can be confused with MS - however Optic neuritis and myelitis tend to more severe in Devic S & brain MRI more normal , CSF fluid - no oligoclonal bands

54
Q

Differiential diagnosis of MS ?

A

Neuromyelitis optica (Denver syndrome )

THESE CAN HAPPEN AFTER INFECTION
(POST- INFECTIOUS AEITOLOGY)
0 Idopathic transverse myelitis (inflammation of spinal cord ) -

0 Acute disseminated encephalomyelitis/ post viral demyelination syndrome - brief attck of inflammation in brain + spinal cord - more likely in children- damages myelin
- happen after viral infection/ vaccination
monphasic - lesions appear but go away and do not come back.
- rapid , with fever , headaches fatigue
- tends to affect temporal lobe & limbic structures - and then spread to other areas.
- can get gyri enhancement & hamorrgae

METABOLLIC DISORDERS
0 Vitamin B12 deficiency
0 Copper defciency

0 Hypothyroidism 0 Hypocalemia
0 Diabetic Peripheral neuropathy
- all have similar sensory symptoms to MS

0 Primary CNS vasculitis.
Ischaemic stroke.

0 Autoimmune condition - endotheliopathy (disease of endothelium )- of small BV supplying brain , inner ear , retina.
Present with:
0 encephalopathy - main problem (this variant solves within 1-3 years and has a relasping - remitting pattern)
- decline in cognitive function , memory etc, gait issues dysarthria
0 deafness/ hearing loss - lower frequncies , sudden.(tinnitus), vertigo
0 branch retinal artery occlusion - but ebcome a problem as recurrent. (cause vision problems - scotoma (curtain over eyes)

(others take longer to resolve - 3-10 years)

Treatment
(Immunosupression)

  • often misdiagnosed as MS.
    (- when it presents with mostly hearing loss, tinnitus & vertigo diagnosed as Meniere’s disease(m)
  • M - often unilateral
    Susac - Bilateral

Systemic inflammatory disorders:
0 SLE — can cause stroke-like episodes.

Behcet’s syndrome — typically presents with a history of oral and genital ulcers, and uveitis. High risk of thrombotic events including cerebral thrombosis.

0 Sarcoidosis — a multi-systemic granulomatous disease that can affect various parts of the body.

0 Primary or metastatic neoplastic brain lesions — (can cause progressive neurological symptoms )

0 Paraneoplastic syndromes — may cause cerebellar ataxia and other neurological symptoms and signs.

INFECTIONS

  • Lyme disease
  • Tertiary syphillis
  • HIV
  • Tropical spastic paraparesis -Human T Lymphotrophic virus.

Optic neuritis - common manifestation of cns inflammation - if history of this - then especially ms or neuromyelitis optica could be possible.

55
Q

Upper motor neurone vs Lower motor neurone lesion.

A

UPPER - up - arrow pointing upwards - increased

More muscle contraction ——–> Spascity

More muscle tone —-> Hypertonicity

More muscle reflexes ——->Hyperreflexia

More Disuse - Disuse atrophy
(cant use them cause they cant bec controlled)

56
Q

Upper motor neurone vs Lower motor neurone lesion.

A

UPPER - up - arrow pointing upwards - increased

More muscle contraction ——–> Spasticity
(Spasticity - velocity dependent resistance to passive stetch - e.g if you move someone arm slowly less resistance than when you move it fast)———————————-> leads to:
claspknife rigidity i.e . movement very rigid and hard at first but gets better after use - passive movement
(this is not rigidity i.e. led pipe rigidity - as rigidity/Resistance to passive movement is there the whole way)

More muscle tone —-> Hypertonicity

More muscle reflexes ——->Hyperreflexia

More Disuse - Disuse atrophy
(cant use them cause they cant bec controlled)
(slight wasting)

increased - claspknife rigidity i.e . movement very rigid and hard at first but gets better after use - passive movement

positive babinski - toes up

LOWER —–> down —-> arrow pointing down ————> decreased

Less muscle contraction ——–> Flacid

Less muscle tone —-> Hyportonicity

More muscle reflexes ——->Hyporeflexia

loss of innervation - Dinnervation atrophy
(Profound wasting)

*absent babinski

*Power is reduced in both
- active resistance reduced.
- flexion at elbows & stronger than extension
- flexion at knee weaker than extension
straight legs, elbows curled up.

(brainstem lesion - cause upper motor neurone signs)

57
Q

Facial nerve - Upper motor neurone vs lower motor neurone ?

A

Facial nerve - Upper motor neurone - bilateral innervation from cortex to upper half of facial nucleui- forehead is spared

Lower motor - no bilateral innervation - so forehead not spared.

58
Q

What is bulbar palsy ?

A

A bulbar palsy refers to disease affecting :
0 Glossopharyngeal - motor innervation to parotid gland
0 Vagus - motor & sensory innervation to organs e.g digestive(stimulate smooth muscle contraction & glandular secretions) - rest and digest.
- motor innervation to muscle of pharynx , soft palate , larynx.
-sensory - taste innervation to tongue
0 Accessory - (Motor innervation of trapezius & sternocleidomastoid)
0 Hypoglossal nerves - Motor innervates tongue
Due to lower motor neuron pathology.

Typically, present with signs and symptoms of the cranial nerves affected as mentioned.

  • dysphagia
  • dysarthria
  • flaccid pareses
  • atrophy
  • fasciculation of muscles supplied by those cranial nerves
  • fibrilliation of the tongue
  • weakness of the palate
  • reduced or absent gag reflex
  • dribbling of saliva and a nasal speech.

The causes of a bulbar palsy can include
o vascular (infarction of the medulla)
o degenerative disease (amyotrophic lateral sclerosis , malignancy (of the brainstem)
o inflammation (e.g. poliomyelitis, Guillain-Barré) o genetic disease

Myasthenia gravis - usually presents with weakness in proximal limbs , trunk , neck etc - commonly also a pure bulbar presentation.

59
Q

What is botulism ?

A

Paralytic illness - Clostridium Botulinium produces neurotoxin - attack brain , spinal cord and nerves causing paralysis and weakness.

DOES NOT CAUSE FEVER!!!!

CHARACTERISED :
0 cranial nerve palsies
0 oculobulbar weakness
0 descending, symmetrical flaccid paralysis in the absence of fever.

Affected patients do not complain of sensory deficits.

SIGNS:
0 Blurred vision
0 Impaired accomodation
0 Ptosis
(paralysis of CN 3,4,6)

0 Ocularbulbar weakness - Ocular (eye) + bulbar weakness
(vagus , glossopharyngeal , hypoglossal , acesssory)
- blurred vision, diplopia, dysarthria, and dysphagia.)
Hypoglossal weakness - tongue.

Affected infants develop feeding difficulties and a weakened cry.

(symmetrical paralysis that spreads down the body from the head to the legs.)

Respiratory dysfunction may result from diaphragmatic and accessory muscle weakness. (uncommon)

Deep tendon reflexes, initially present, diminish or disappear within a few days of infection.

AUTONOMIC DYSFUNCTION - 
0 Postural hypotension
0 dry mouth and throat
0 constipation - presents in 95% of infants. 
0 Urinary rentention
0 hypothermia

RISK FACTORS
- Ingestion of contaminated food
- Infantile age group
- Biological terrorism
WEAK
- ingestion of honey (now discouraged), soil in infants
- exposure to reptiles
- therapeutic use of botulinum toxin (iatrogenic)
- IV drug usage (wound botulism ) - also crush injury - infected wound.

TESTS

  • Mouse bioassay (gold standard)- patients’s serum , gastric secretions , stool or food sample injected into mouse to show sigs of symptoms caused by parasite.
  • serum , stool , gastric secretions, food culture.

Electrophysiological testing - This test is very uncomfortable and should not be requested unless botulism or Lambert-Eaton myasthenic syndrome is a serious consideration.

MAIN TREATMENTS
- Rapid administration of Botulism antitoxin.
under 1 year:
- Rapid administration of Botulism immunoglobulin
FOOD BOURNE
- Gastric lavange - remove unabsorbed toxin
WOUND Antibiotics and debridement(form of cleaning if wound)

60
Q

What test would you do if you were concerned about respiratory weakness ?

A

Respiratory muscle weakness gives results on spirometry similar to a restrictive deficit, since in both cases the lungs cannot be inflated sufficiently. The best ward-based measure of this is the FVC; sniff pressure is also a good test but is not routinely available on wards.

Tidal volume might be reduced but is not sufficiently sensitive.

The FEV1, FEV1/FVC ratio and PEFR are sensitive to airway obstruction, not restriction.

61
Q

What is bells palsy ?

A

Damage to the facial nerve after it leaves the internal acoustic meatus.
(can be cause by acoustic neuroma (when travelling from pons to internal acoustic meatus ) or while travelling through facial canal - inflammaton etc. , tumor in patotid gland compressing nerve.

It affects the ipsilateral side the lesion is on

causes:

facial dropping of one side - LMN lesion
(upper & lower parts face affected including forehead)

forehead sparing - UMN neurone lesion - as forehead is the only part that has bth contralateral & ipsilateral innervation
https://www.youtube.com/watch?v=qgO8Vhij758l
look at 7 mins - for umn vs lmn

AMK (92 decks)

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