6.1.14 Assesses signs and symptoms of neurological significance. Flashcards
General symptom of neurological condition
- Reduced vision / transient loss of vision
- Headache
- Loss of VF
- Pupil abnormality
- Diplopia
- Dyschromatopsia - mainly R/G, so test Isihara monocularly
- Diminished light brightness sensitivity , desaturated red can combine this aspect & red green deficiency
Tests to do for neurological:
- History & symptoms – headaches, visual symptoms, sudden loss of vision
- VA
- Pupils
- Motility / CT
- Stereoacuity?
- Fundus exam
- Including spontaneous venous pulsation test
- VF test
- Amsler
- Colour vision
- Check for red desaturation
- City to include tritan
- Contrast sensitivity
Optic nerve dysfunction, expect:
- Reduced VA – D&N
- Impaired CV – R/G or B/Y
- RAPD
- VF defect
- Impaired CS
*
Differential diagnosis of raised optic disc
Optic disc oedema
* Papilloedema
* Anterior ischemic optic neuropathy
* Optic neuritis
Compression of optic nerve
* Infiltration of the optic nerve
* Congenital optic neuropathies
* Toxic optic neuropathies
* Traumatic optic neuropathies
(Raised but no swelling)
* Optic disc drusen
* Tilted optic disc
* Myelinated nerve fibres
* Hypermetropic crowded disc
Intraocular disease which can cause raised disc appearance
* CRVO, posterior uveitis, posterior scleritis, hypotony
Excavated disc anomalies
* Optic disc pit
* Coloboma
* Optic nerve hypoplasia
* Morning glory anomaly
Optic disc oedema
Characteristic appearance of the optic nerve head:
- Elevated appearance of nerve head
- Filling of cup
- Retinal vessels drape over disc margin
- Blurring of margin
- RNFL oedema – greyish appearance that obscures vessels
- Hyperaemia – BV swollen, redness
- Retinal venous dilatation & tortuosity
- Peripapillary haemorrhages, exudates, cotton wool spots
Papilloedema
Swelling of the optic nerve head secondary to raised ICP
Causes
* Intracranial mass
* Hydrocephalus (dilation of ventricles)
* Central nervous system infection e.g. meningitis
* Trauma
* Infiltration e.g. leukaemia, sarcoidosis
* Benign intracranial hypertension (only benign when all other causes are absent) – most common in overweight, middle aged women
Papilloedema
Symptoms
- Occasionally asymptomatic (could be picked up in routine eye exam)
- Nausea and vomiting – projecticle vomiting
- Deterioration of consciousness – from slight (drowsy) to dramatic
- Pulsatile tinnitus
- Can be ‘muzzy headed’ at start and then develop into extreme pain, usually presenting at hospital within 6 weeks
- Characteristically in morning, waking up px
- Generalized or localised
- Headaches worse when pressure increases - moving head, bending over, coughing
*
Papilloedema
Visual symptoms
- (only after some time i.e. in established cases)
- Visual symptoms often absent but reduced VA in later stages
- Transient visual loss (especially when bendning over)
- Horizontal diplopia (6th nerve palsy)
- Constriction of visual field
- Altered colour perception
Signs of Papilloedema
EARLY – first few weeks
* VA normal
* Optic disc shows Hyperaemia, mild elevation and indistinct margins
* Dilation of capillary net
* Absent SVP (absent in 20% normals)
ESTBALISHED ~ 6 months
* VA normal or reduced
* Optic disc shows venous engorgement, moderate elevation, flame-shaped haemorrhages and cotton wool spots
* Enlarged blind spot
* Hard exudates in macular fan
CHRONIC > 6 months
* VA is variable
* Optic discs are pale and markedly elevated
* No haemorrhages or cotton wool spots
* Collateral vessels form
* Variable field loss
ATROPHIC – years after initial presentation
* VA severely impaired
* Fields impaired
* Optic discs are pale grey and slightly elevated with indistinct margins
papilloedema
OCT
- RNFL white showing raised
- Can use measurement tools on OCT to measure disc swelling (>400 microns indicate a swollen disc)
papilloedema
Management (CMGS)
- Communicate severity of situation to px
- Phonecall to ARC
- Emergency referal to ophthalmology/neurology with letter in hand
- Younger px = less likely to be bengin
- Treatment of cause at HES
- Carbonic anhydrase inhibitor to reduce ICP in IIH
AION types
- **Inflammation of ON due to ischaemia **
Arteritic (AAION)
* Occurs in >70s
* Caused by giant cell arteritis
* Associated systemic features e.g. hard temporal artery, scalp tenderness, jaw claudification, muscle weakness, reduced appetite
* Severe vision loss (poorer than 6/60)
* Pale swollen disc, cotton wool spots, RAPD
* Stroke risk high: high chance of 2nd eye being affected
Non-arteritic (NAION)
* Occurs in >60s
* Caused by occlusion of short posterior arteries (RF’s: DM, HBP, smoking)
* No systemic features
* Mod-severe loss of vision (better than 6/60)
* Hyperaemic swollen disc, peripapillary flame shaped haems
* Lower risk
AAION (GCA)
Risk factors
- Hypertension
- Smoking
- Diabetes
- Stroke
- Sleep apnoea
- Anaemia
AAION (GCA)
Symptoms
- Sudden, profound unilateral visual loss
- May be proceeded by transient visual obscuration (amaurosis fugax), flashing lights
- Periocular pain
- Systemic – headache, pain in the neck & temples, weight loss, fatigue, scalp tenderness, jaw claudication
AAION (GCA)
Signs
- VA HM to no PL
- Pale swollen disc
- Peripapillary haemorrhages
- Cotton wool spots (signifying retinal ischaemia)
- RAPD
AAION (GCA)
Management
- Emergency referral to ophthalmology
- Sight-threatening nature, and to administer prompt treatment with the aim of preventing blindness to the 2nd eye
- Temporal artery biopsy
- Vision lost usually permanent
- Prompt administration of steroids (with gastric protection) may allow for partial visual recovery
- Iv methylprednisolone 500m to 1g/day for 3 days, followed by oral prednisolone for 3 days
- Treatment continued until symptom resolution and ESR normalization, or 4 weeks
- In 25% cases 2nd eye is affected despite treatment/steroid administration– within a few days
describe NAION
- Inflammation of optic nerve due to ischaemia, not related to inflammation of arteries
Causes - Drop in BP
- Increase in blood viscosity
- Reduced blood flow around nerve
- Most AION’s are non-arteritic - 90% of AION cases
NAION
Risk factors
- Structural crowding of disc - cup is small/absent
- Common modifiable risk factors include DM, HBP, high cholesterol, smoking
NAION
Symptoms
- Sudden, painless unilateral vision loss, Over hours - days
- Often described as a blurring or cloudiness of vision
- Px may also report H/A (8-12% px’s)
NAION
Signs
- VA 6/18 to CF , May only be slightly reduced/normal in some individuals
- Diminished colour vision
- Hyperaemic, swollen disc with a few splinter shaped haemorrhages
- Altitudinal hemianopia – most commonly inferior
- Fellow eye has smaller or absent cup
NAION
Management
- Emergency referral to ophthalmology
- Sudden loss in vision warrants emergency referral according to CMGs
- No definitive treatment, some advocate short-term systemic steroid treatment
- Treatment of any underlying systemic predispositions
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Describe Posterior Ischaemic Optic Neuropathy (PION)
- Much rarer than AION
- Caused by ischaemia of the retrolaminar portion of the optic nerve supplied by the surrounding pial capillary plexus, which in turn is supplied by the plial branches of the ophthalmic artery.
- Diagnosis made only after other causes of retrobulbar optic neuropathy have been excluded (e.g. compression, inflammation
Describe Optic neuritis
Acute or subacute inflammatory or demyelinating process affecting the optic nerve
Optic neuritis
Ophthalmology classifications
Retrobulbar neuritis – normal appearance of the OD, at least initially
* Most common type in adults
* Frequently associated with MS
* Other causes: tuberculosis, syphilis, viral infections
Papillitis – disc hyperaemia/oedema, occasionally PP flame-shaped haemorrhages
* Most associated with diabetes
Neuroretinitis – papillitis and a macular scar
* 66% caused by cat scratch
Optic neuritis
Aetiology classification
Demyelinating (MS)
Para-infectious
Infectious (Cat-scratch)
Non-infectious/autoimmune (DM)
Retrobulbar neuritis
- Demyelination may be caused by MS or be idiopathic, usually, age range 20-50 years,
- 75% patient’s female
Retrobulbar neuritis
Symptoms
- Subacute monocular (usually) vision loss; typically progresses over less than 7 days
- Some patients experience tiny white or coloured flashes/sparkles (phosphenes)
- Pain on eye movement
- Frontal H/A and tenderness of globe may be present
Retrobulbar neuritis
Signs
- VA 6/18-6/60, rarely worse
- Impaired colour vision / red desaturation
- RAPD if unilateral
- VF defect; central scotoma
- Disc appearance normal or swollen, pale optic nerve & veins
*
Retrobulbar neuritis
Management
- Urgent referral to HES – CMGs + GGC
- Confirm diagnosis – MRI/CT
- High dose IV steroids (prednisolone) within first week of symptoms onset = better prognosis
- Systemic investigation to determine if underlying MS
Differential Diagnosis of Different Neurological Conditions
- INFLAMMATORY - Optic Neuritis; this includes demyelinating, parainfectious, infectious & non-infectious & neuroretinitis
- PAPILLOEDEMA - secondary to increased intracranial pressure
- ISCHAEMIC - Anterior non-arteritic, anterior arteritic, posterior ischaemic and diabetic papillopathy
- COMPRESSIVE - Secondary to Orbital lesion
- INFILTRATIVE - Inflammatory conditions (e.g. sarcoidosis), tumours and infective agents
- TRAUMATIC
- HEREDITARY - Leber & other ones
- NUTRITIONAL & TOXIC
Tumours & Compressive Lesions
- Pituitary
- Bitemporal hemianopia
- Frontal HA - gradual onset of symptoms
- Desaturated red - across vertical midline from nasal to temporal comparison for each eye suggests compression
- Optic atrophy possible
Management
* Depends on extent, generally urgent if a lot of vision loss. Soon within a month if very subtle signs
* MRI done
* Radiation modulated radiation therapy
Optic Nerve Sheath Meningioma
- Neoplasms from meninges of surrounding ON
- Women 3:1, 4-5th decade of life
- Monocular vision loss - depends on extent
- Other neuro problems - RAPD, CV defec, VF loss, Optic atrophy/oedema/optociliary shunt
Management
MRI, Radiation therapy
3rd Nerve
- Can either be affecting superior or inferior division
- Superior = SR + Levator
- Inferior = IO, IR, MR
- What does it look like?
- Primary position - ExoT & HypoT, Ptosis
- Abduction is AOK, Adduction is not
- Limited elevation & depression
- Pupil dilation (if pupillary involvement - this is really bad for the px!)
- Causes - M (microvascular) A (aneurysm) T (trauma) E (episodic)
- Management - urgent referrral within 1 week, emergency if pupil involvment as could be aneurysm
4th Nerve
- SO affected
- What does it look like?
- Primary position - HyperT, Head tilt & chin depression
- Adduction causes IO overaction, Abduction AOK
- Limited depression on adduction
- 3 Step Test
1. Look at primary position: affected eye has HyperT
2. WOOG - worse on opposite gaze. Deviation will increase
3. BOOT - better on opposite tilt. Deviation will increase on same side tilt
6th Nerve
- Abducens nerve
- What does it look like?
- Marked EsoT
- Adduction AOK, Abduction limited
7th Nerve ( Bells Pallsy)
Which parts of the face are innervated?
Lacrimal Gland Obicularis oculi muscle (palpebral, orbital & lacrimal) Nose, Jaw
What is the main cause?
Cause unknown, most **idiopathic** Otherwise, separate conditions like infection, trauma, tumour may cause nerve paralysis
Symptoms
Cosmesis of face messed due to change in muscle tone Eye watering Ocular exposure means redness, pain, photophobia, reduced vision
Signs
Incomplete blink - corneal drying Prolonged exposure - incomplete closure at night Eye watering - lacrimal pump function reduced Conjunctival hyperaemia, staining, oedema (sometimes inferior ulceration)
Management
Tape lids closed at night Sunspex for photophobia & protection Lubricants!! **Referral:** - New cases, and where there is loss of corneal sensation: **A2: first aid measures and emergency (same day) referral to GP or hospital A&E department** - Recovering and established cases: **B2: alleviation/palliation; no referral** - If cannot be managed easily, then: **B1: prescription of drugs; routine referral**
