Neuro Table Flashcards
Infective Conjunctivitis
Self-limiting bacterial or viral infection of the conjunctiva. bacteria / virus. bloodshot, burn or feel gritty, produce pus that sticks to lashes, itch, No loss of vision as long as infection does not spread to cornea. “antibiotic eye drops if likely to be bacterial.
gently rub eye lashes to clean off crusts, hold a cold flannel on your eyes for a few minutes to cool them down” infectious - can spread to others
Allergic Conjunctivitis
allergy Itchy, Red, Discharge (mucoid/watery), Acute, Lid swelling, chemosis “Topical antihistamine
- Avoid allergen
- Mast cell stabilisers - sodium cromoglycate – prophylactic treatment”
Corneal Abrasion
trauma Pain, Watering, Blurred vision, Epithelial defect “slit lamp
- staining with fluorescene “ “Topical antibiotics
- Analgesia - Examination almost impossible until topical anaesthetic. - can’t give them it to manage pain because it delays healing, so just OTC meds. “ Heals very quickly – quite a lot better in 24hrs, pretty much fully in 48
Corneal ulcer
an open sore on the cornea infection, physical and chemical trauma, corneal drying and exposure, and contact lens overwear and misuse, corneal degenerations or dystrophy. “Feeling of something in eye
Grey or white spot on the cornea
Eye inflammation or redness
Eye pain or discomfort
Eye discharge
Blurred vision
Sensitivity to light” ophthalmologist referral. Look with slit lamp. Fluorescene. Needs aggressive management to prevent spread, scarring. medicated eye drops to treat the bacterial or viral causes. Stop spread of infection. Cool compress. Corneal transplant. partially or completely blind in a very short period of time. Your cornea may also perforate, or you could develop scarring, cataracts, or glaucoma.
Cataracts
the lens, a small transparent disc inside your eye, develops cloudy patches. Older (embryological, foetal) fibres are never shed – compacted in the middle “age.
Risk:
A family history of cataracts, Smoking, Regularly drinking excessive alcohol, A poor diet lacking in vitamins, Lifelong exposure of your eyes to UV light, Taking steroid medication over a long time, Previous eye surgery or injury, diabetes. Blurred, misty or cloudy vision, more difficult to see in dim or very bright light, Bright lights dazzling or uncomfortable to look at, Colours look faded or less clear with a yellow or brown tinge, double vision, see a haloes (circles of light) around bright lights “surgery- Topical anaesthetic.
No stitches – slanted incision. New eye drops that may decrease the opacity. “
Glaucoma (Primary Open Angle Glaucoma (POAG))
open, normal appearing anterior chamber angle and raised intraocular pressure (IOP), with no other underlying disease. progressive condition and is the most common cause of irreversible blindness worldwide. something is wrong with the ability of the cells in the trabecular meshwork to carry out their normal function, or there may be fewer cells present, but not really known. Patient can be asymptomatic for a long period of time. altered field of vision (arcuate scotoma). Raised IOP. Bilateral. Pressure on optic nerve head as nerve fibres die out. When seen by ophthalmoscopy – optic disc appears unhealthy, pale and cupped. Loss of neuroretinal rim Picked up on routine eye exams, Air puff test. “Eye drops to decrease IOP
(Prostaglandin analogues,
Beta-blockers,
Carbonic anhydrase inhibitors)
Laser trabeculoplasty
Trabeculectomy surgery. can cause blindness
Acute Angle Closure Glaucoma
rapid or sudden increase in pressure inside the eye. Pressure can be up to 70mmHg. “Functional block in a small eye – large lens
Mid-dilated pupil - periphery of iris crowds around angle and outflow is obstructed
Iris sticks to pupillary border (synechia) which prevents reaching AC. Leads to iris balooning anteriorly and obstructing angle. Older people more at risk – lens is bigger – smaller angle
Hypermetropia - swallower angle” “Pain++
-Redness
-Blurred vision
-Nausea & vomiting
-Hazy cornea
-Fixed mid dilated pupil - the position in which the obstruction is most likely to occur
-Hard eyeball” “Red eye, cornea often opaque as raised IOP drives fluid into cornea. AC shallow, and angle is closed.
Pupil mid-dilated (fixed)
IOP severely raised” Slit-lamp photo showing shallow AC “Decrease IOP
(IV infusion with or without oral therapy – carbonic anhydrase inhibitors (acetazolamide),
Analgesics, antiemetics,
Constrictor eye drops – pilocarpine,
If no contraindication beta-blocker drops such as timolol,
Steroid eye drops (dexamethasone))
Iridotomy (laser) - both eyes - to bypass blockage” blindness
Uveitis
“inflammation of the middle layer of the eye, called the uvea or uveal tract. Anterior uveitis – iris with or without ciliary body inflammed
Intermediate uveitis – ciliary body inflammed
Posterior uveitis – choroid inflammed” “Isolated illness
Non-infectious autoimmune causes – eg: presence of HLA-B27 predisposes to anterior uveitis
Infectious causes – chronic diseases such as TB
Associated with systemic diseases – eg: ankylosing spondylosis “ Pain, dull ache around eye - worse when focusing, watering, eye redness, photophobia, blurred or cloudy vision, floaters, loss of peripheral vision, Small irregular pupil, May have previous history “An inflammed anterior uvea (iris) leaks plasma and white blood cells into the aqueous humor - hazy AC, cells deposited at back of cornea - Keratic precipitates – white spotty appearance. Hypopyon. In intermediate uveitis the ciliary body is inflammed and leaks cells and proteins.
This leads to a hazy vitreous. In posterior uveitis the choroid is inflammed.
Since the choroid sits under the retina, the inflammation frequently spreads to the retina causing blurred vision” “corticosteriods.
eyedrops are often used for uveitis that affects the front of the eye (anterior) - Dilating drops - Cyclopentolate
injections, tablets and capsules are usually used to treat uveitis that affects the middle and back of the eye (intermediate and posterior) eyedrops, immunosuppressants, surgery” recurrent or chronic. Glaucoma, detatched retinas, cataracts, cystoid macular oedema, posterior synechiae
Myopia
shortsightedness Eyeball is every so slightly longer than normal (most common cause) Image is formed a bit to early, in front of the retina, rather than on. Close objects look clear, distant objects appear hazy, headaches “Complain of not being able to see blackboard/ distant objects.
Infants & preverbal children - divergent squint
Toddlers - loss of interest in sports/people. More interest in books, pictures.
Teachers may notice child losing interest in class.” eye test “treat seriously in children. Biconcave lenses
-Spectacles
-Contact lenses
-Laser eye surgery” squint, accidents due to poor vision
Hyperopia
farsightedness Eyeball too short or cornea + lens too flat. Close objects look hazy, distant objects appear clear. Symptoms of eyestrain after reading/ working on the computer in a young individual. Convergent squint in children/ toddlers – needs immediate correction with glasses/lenses to preserve vision in both eyes and prevent a “lazy eye”. eye test “Biconvex glasses alleviates use of glasses for focussing distant objects and ‘rests’ the accomodative power
Contact lenses
Laser Eye surgery” lasy eye. Accidents from poor vision
Astigmatism
Close and distant objects appear hazy Surface has different curvatures in different meridians eye test cylindrical glasses (which are curved in only one axis). Laser eye surgery, toric contact lenses.
Presbyopia
longsightedness of old age. “With age the lens gets less mobile/elastic.
So when the ciliary muscle contracts, it is not as capable as before to change shape.
So seeing near objects/ reading the newspaper starts to become difficult - needs glasses to read.” progressive difficulty with close up objects from 5th decade onwards eye test needs biconvex - reading glasses
Vitamin A deficiency
lack of vitamin A - 6 months store in liver is depleated. can occur in conditions such as malnutrition, malabsorption syndromes such as coeliac disease, sprue. night blindnesss Vitamin A is also essential for healthy epithelium. So conjunctiva and corneal epithelium are also abnormal. Bitot’s spots in conjunctiva, Corneal ulceration blood test. “Corneal melting
Which leads to future opacification of the cornea”
Strabismus (Squint)
Esotropia (manifest convergent squint)
Exotropia (manifest divergent squint)
glasses and treat underlying issues
Amblyopia
lazy eye. where brain supresses the image of one eye leading to poor vision in that eye without any pathology functional consequence of a squint correctable in early years using eye patches to stimulate the “lazy” eye to work constant lazy eye
Diplopia
double vision usually occurs in squints occuring as a result of nerve palsies. monocular - dry eye syndrome, astigmatism, cataracts, keratoconus Double vision affecting both eyes is usually a symptom of a squint.
Retinal Detatchment
the inner 9 layers become detached from the outer most 10th in trauma vitreous humor filling/pushing the potential space open when there is a tear. Can also just happen with changes in vitrous humour volume/components. Also scar traction, tumours and imflammation. “ floaters
flashing lights
a dark shadow in your vision
blurring of your vision.” retinal examination surgery, pneumatic retinopexy, scleral buckling, vitrectomy loss of some or all of vision
Insomnia
chronic inability to obtain the necessary amount or quality of sleep to maintain adequate daytime behaviour “chronic, primary insomnia where there is usually no identifiable psychological or physical cause
temporary, secondary insomnia in response to pain, bereavement or other crisis. Usually short lived.” lack of sleep, waking up loads, taking ages to get to sleep. Tired, irritable, lack of concentration, needing to nap. “Benzodiazepines. Pharmacy treatments. Try and manage
stress, anxiety or depression
Reduce noise, a room that’s too hot or cold, uncomfortable beds, alcohol, caffeine or nicotine, recreational drugs like cocaine or ecstasy, jet lag, shift work” Benzodiazepines - very addictive.
Nightmares
have a strong visual component and are seen during REM sleep typically occurring quite far on through the night, Waking will stop the nightmare and the individual will have a clear recollection of the “dream” counselling if needed. But try figure out if theres any issues
Night terrors
sleepwalking behaviour type “nightmare”. Their eyes will be open, but they’re not fully awake. common in children aged between 3 and 8 years old. More common when tired, fever or certain types of medication, or anxious, needing the toilet. occur in deep, delta sleep, may scream, shout and thrash around in extreme panic, and may even jump out of bed The episodes usually occur in the early part of the night, continue for several minutes (up to 15 minutes), and sometimes occur more than once during the night don’t wake them, unless they are in danger. Try waking them before episodes if they have a timing pattern to try break the cycle.
Somnambulism
Sleep-walking occurs exclusively in non-REM sleep, mainly in Stage 4 sleep and is more common in children and young adults, probably due to the decline in Stage 4 sleep with age walk with their eyes open, can see and will avoid objects, can carry out reasonably complex task such as prepare food and will often obey instructions but have no recall of the episode when woken. prevent triggers, lack of sleep, stress, anxiety, fever, alcohol, recreational drugs, sedatives, needing to go to the toilet during the night for some reason. hurting themselves when asleep
Narcolepsy
suddenly fall asleep at inappropraite times. Patients enter directly into REM sleep with little warning. Linked to dysfunctional orexin release from the hypothalamus. Immune system sometimes invloves in attacking the area where its released. excessive daytime somnolence, cataplexy, sleep paralysis, sleep attacks, headaches, hallucinations, memory troublem depression, restless sleep Symptoms could be interpreted as intrusion of REM sleep characteristics onto the waking state sleep analysis, blood tests, lumbar puncture for orexin. Very dangerous because of accident risk if e.g. driving.
MS (multiple sclerosis)
central nervous system, demyelinating disease. Can be relapsing remitting, secondary progressive or primary progressive “more common in people in 20s/30s, and women and temperate climates. Auto immune process (more common in those with other autoimmune conditions)
-Activated T cells cross blood brain barrier causing demyelination
-Acute inflammation of myelin sheath
-Loss of function” “
fatigue, vision problems, numbness and tingling, muscle spasms, stiffness and weakness, mobility problems, pain,
problems with thinking, learning and planning, depression and anxiety, sexual problems, bladder problems, bowel problems, speech and swallowing difficulties” “Lesions or plaques on MRI scan (white blobs). Later - Black holes on MRI
-Later seen as cerebral atrophy (Sulci look too big) Optic neuritis
-Sensory symptoms – numbness, pins and needles
-Limb weakness – can be one or both etc.
-Brainstem affected - Diplopia/Vertigo/Ataxia
-Spinal cord affected -bilateral symptoms and signs +/- bladder (incontinence) “ “MRI. Examination: Afferent pupillary defect - Sign of previous optic neuritis.
-Nystagmus or abnormal eye movements
-Cerebellar signs
-Sensory signs
-Weakness
-Spasticity
-Hyperreflexia
-Plantars extensor Lumbar Puncture, bloods, vision / somatosensory tests, CXR, look for infection in relapses “ oral/IV prednisolone, rehab, symptomatic treatment. Beta-interferons, glatiramer acetate, Teriflunomide, Dimethyl Fumarate, Natalizumab, Fingolimod, Alemtuzumubm, MDT. prognosis uncertain. Post inflammatory gliosis - may have functional deficit. Some treatments carry a small risk of PML.
Neuromyelitis Optica Spectrum Disorder (Devic’s Disease)
Optic neuritis - bilateral and severe – don’t get full recovery.
- Myelitis
- Aquaporin-4 antibodies
- Antibody negative in some cases
OPTIC/ RETROBULBAR NEURITIS
It is also known as optic papillitis (when the head of the optic nerve is involved) and retrobulbar neuritis (when the posterior part of the nerve is involved). demyelination within the optic nerve “Subacute visual loss
monocular visual loss
-pain on eye movement
-reduced visual acuity
-reduced colour vision -Usually resolves over weeks
“ “Initial swelling optic disc
-Optic atrophy seen later” fundoscopy. VEP. Visual evoked response – how the optic nerve is firing. Can pick up issues even if they’ve been asymptomatic.
Demyelinating Myelitis
Demyelination or inflammation within the spinal cord Usually part of multiple sclerosis. Can affect the young “Sensory level often with band of hyperaesthesia
-Weakness/ upper motor neurone changes below level
-Bladder and bowel involvement (urinary retention)
-May be painful, Subacute onset, There may be a history of previous neurological or ophthalmological episodes” Partial or Transverse (complete). pathological lesions of inflammation and demyelination leading to temporary neuronal dysfunction MRI, CSF “Supportive
Methylprednisolone” “May have a chronic progressive myelopathy
2˚ or 1˚ progressive”
contralateral homonymous hemianopia
Vascular and neoplastic (malignant or benign tumours) lesions from the optic tract, to visual cortex. (optic radiation) can’t see out of lateral aspect of one eye and medial of other. Brain is damaged on opposite side as where you get the lack of vision (lateral of right eye - left side damaged) Left sided lesion – right visual field loss visual field testing
bitemporal hemianopia
can’t see out temporal aspects of both eyes Optic chiasma disrupted in the middle. Can be pituitary tumour. can’t see lateral aspects from both eyes visual field testing
Stye / hordelum
An external stye (hordeolum externum), An internal stye (hordeolum internum). a bacterial infection of an oil gland in the eyelid. bacteria a small, painful lump on or inside the eyelid or around the eye, skin may be red, swollen and filled with yellow pus like a pimple, watery eyes but vision should not be affected “common and should clear up on their own within a week or two.
Soak a clean flannel in warm water, Hold it against eye for 5 to 10 minutes, Repeat this 3 or 4 times a day. surgical incision and curettage” spread
coloboma
congenital malformation of the eye causing defects in the lens, iris, or retina. congenital, parts of the eye don’t form properly and close up together mild to more severe visual loss depending on what part of the eye is affected keyhole like shape in the pupil “May have other issues: C - coloboma
H - heart defects
A - atresia of the choanae (problems with the nose passages)
R - retarded growth and developments
G - genital hypoplasia (undescended testicles)
E - ear abnormalities.” no treatment. Sunglasses for light sensitivity, glasses for non condition related vision problems (maximise good vision) glaucoma, retinal detachment
Cavernous sinus thrombosis
formation of a blood clot within the cavernous sinus can develop when an infection in the face or skull spreads to the cavernous sinuses. The blood clot develops to prevent the infection spreading further. Sometimes, clots can develop without infection. Sinusitis, a boil. Head injury, conditions/drugs that increase chances of blood clots. “a sharp and severe headache, particularly around the eye,
swelling and bulging of the eyes – this usually starts in one eye and spreads to the other eye soon after, red eyes, eye pain – which can be severe, vision problems – such as double vision or blurred vision, difficulty moving the eyes, ptosis and mydriasis” “a high temperature of 38C or above
vomiting
seizures (fits)
changes in mental state, such as feeling very confused. papilloedema and/or retinal-vein dilatation
decreased corneal reflex
hypo- or hyper-aesthesia in the distribution of the ophthalmic and maxillary nerves” FBC, blood culture, MRI, CT, possibly lumbar puncture antibiotics, anticoagulants (heparin and further tablets for a few months), corticosteriods, surgical drainage of infection site it can restrict the blood flow from the brain, which can damage the brain, eyes and nerves running between them. Without treatment can go into a coma. Vision loss, further infections, other blood clots. ICA is in the cavernous sinus – can get communication of venous and arterial system.
Blow out fracture of the orbit
a traumatic deformity of the orbital floor or medial wall typically resulting from impact of a blunt object larger than the orbital aperture, or eye socket “one eye isn’t moving up.
Has to be superior rectus or inferior oblique. But other muscles are ok – so points out its probably not an issue with a nerve. (III). Infraorbital nerve can be affected. Loss of sensation below eye of affected side” “fat or muscles can herniate out and get caught up in the fracture.
If on the floor – the inferior muscles will be tethered/caught in the fracture – muscles can’t elevate the eye. “ Teardrop sign. (maxillary sinus). On CT
3rd nerve palsy
“Is the 3rd nerve palsy pupil sparing or not.
If it is – more likely medical cause – like diabetes.
If it isn’t – more likely compression – cerebral artery aneurysm?? – immediate investigation. “ eye down and out. Ptosis. headaches, sudden onset of double vision
4th nerve palsy
Cant look towards nose – Superior oblique affected.
6th nerve palsy
can’t abduct eye
Korsakoff syndrome
chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1) most commonly caused by alcohol misuse. Can also be associated with AIDS, chronic infections, poor nutrition. Thiamine (vitamin B-1) helps brain cells produce energy from sugar. When levels fall too low, brain cells cannot generate enough energy to function properly. often preceded by an episode of Wernicke encephalopathy, which is an acute brain reaction to severe lack of thiamine. Wernicke encephalopathy is a medical emergency that causes life-threatening brain disruption, confusion, staggering and stumbling, lack of coordination, and abnormal involuntary eye movements. problems learning new information, inability to remember recent events and long-term memory gaps clinical diagnosis oral thiamine, other vitamins and magnesium 25 percent of those who develop Korsakoff syndrome eventually recover, about half improve but don’t recover completely, and about 25 percent remain unchanged.
Scleritis
serious inflammatory disease that affects the white outer coating of the eye The disease is often contracted through association with other diseases of the body, such as granulomatosis with polyangiitis or rheumatoid arthritis “Pain++ - Deep gnawing pain – radiates into orbit – can’t sleep.
-Redness (deep scleral vessels)
“ “Nodule (does not move over sclera)
-Tender++” Systemic steroids - Need to be admitted – IV prednisolone. Or oral in less severe – but high dose steroid. sight threatening
Orbital Cellulitis
infection of orbital tissues Sinuses normally the root cause of the infection that then tracts into the orbital tissues. Pain+, Redness, Blurred vision, Diplopia, Malaise, Pyrexia, Proptosis, Reduced eye movement, Chemosis CT Scan “Admit
- IV antibiotics
- Drainage of pus” Can lead to meningitis, encephalitis, cavernous sinus thrombosis, blind
Central retinal artery occlusion
occulsion of an artery in the eye Embolus from elsewhere in the body. Most common embolus source – the carotid. - Other common place – heart. AF. “Pupil will not constrict in bad eye (no indirect either) – afferent problem
- Blood vessels look tatty – segmental.
- Retina looks pale and boggy
- Fovea looks cherry red. “ Retina is ischemic – photoreceptors stop working – no sight “Listen for bruits / send for a duplex scan.
- fundoscopy “ Must ensure treatment of risk factors – blood thinners, statin. Unless you see px in 30min, then unlikely to do anything to save sight in that eye.
Central retinal vein occlusion
obstruction of vein in the eye Vein usually obstructed as it passes down through the optic cup. vein compression from artery (they share a common sheath) – in hypertensives Bleeding into the retina – affects vision Fluid seeps out and may get fluid at the macula. – black cystic spaces on imaging (OTC) – damaging of photo receptors OTC Treat risk factors – bp control, assess for hyper viscosity syndromes. intravitreal anti Vegf if you leave the fluid there – permanent vision issues.
Anterior Ischaemic Optic Neuropathy: Arteritic: Giant Cell Arteritis
Inflammatory process of the wall of the blood vessel that thickens the wall. Short posterior ciliary arteries – optic nerve head infarcts. loss of vision, classic headache, sore to brush hair, scalp tenderness, loss of appetite, pain on chewing “tenderness over STAs, raised inflammatory markers - Erythrocyte segmentation rate (ESR) and CRP raised.
-Afferent pupillary defect” ESR and CRP. May need to do a temporal artery biopsy, if unsure. High dose systemic steroids, normally IV - If they’ve infarcted one, then the other optic nerve likely
Non arteritic
Ischemia to the optic nerve.
due to non-inflammatory disease of small blood vessels. Smoking can elevate risk” painless, loss of vision
Age Related Macular Degeneration (AMD)
a common condition that affects the middle part of your vision. It usually first affects people in their 50s and 60s. It’s been linked to smoking, high blood pressure, being overweight and having a family history of AMD “Progressive loss of central vision
-distortion. Condition is bilateral but not necessarily symmetrical”
loss of some but not all of vision
Dry AMD
distortion on amsler chart. Drusen (yellow or white dots), pigment epithelial changes and photreceptors - will see choroid. OCT “No curative treatment.low vision aids
registration”
Wet (neovascular) AMD
distortion on amsler chart. Often a gradual deterioration and a sudden loss (a bleed) OCT. Breach of pigment epithelium, neovascular membrane leaked fluid or blood into retina. Flurescein angiography – see leaks “intravitreal antivegf – monthly injection (Topical anaesthetic – only feel pressure) - Neovascular membranes resolve.
But over the years their vision is likely to deteriorate.
-low vision aids
-registration”
Diabetic Retinopathy
a complication of diabetes, caused by high blood sugar levels damaging the back of the eye (retina) diabetes can cause blindness “microaneurysms
-retinal haemorrhages and exudates
-neovascularisation (disc/retina) - ischemic retina produces vascular endothelial growth factor- leaky - may have a bleed into the vitreous. “ “Flurescein angiography – see leaks
-Fundoscopy – microhaemorrhage loss of capillary beds, bloody looking
-OCT - If they leak – get fluid in the retina – cystic spaces.
Pigment epithelium looks healthy- but leakage of fluid from capillaries.” “intravitreal antivegf - Fluid absorbs and dries out
-laser – panretinal photocoagulation - Laser burns – destroying the peripheral ischemic retina – so less growth factor is produced. Still gold standard treatment.
May give injections then laser to cover the interim
-low vision aids
-registration” commonest cause of visual impairment in working age population
Guillain-Barré syndrome
Guillain-Barré (pronounced ghee-yan bar-ray) syndrome is a very rare and serious condition that affects the nerves. “chances of it increase as you get older. thought to be caused by a problem with the immune system - attacks the nerves. Triggers:
food poisoning – (especially Campylobacter), flu, cytomegalovirus, glandular fever, HIV, dengue, Zika virus” “numbness
pins and needles
muscle weakness
pain
problems with balance and co-ordination. Later - problems swallowing, double vision, walking, speaking, toilet “ no, or reduced reflexes electromyography (EMG), nerve conduction studies, lumbar puncture, Intravenous immunoglobulin (IVIG), plasma exchange, supportive (ventilator, feeding) Guillain-Barré syndrome usually reaches its most severe point within four weeks. It may then remain stable for a few weeks or months before gradually improving. Can be left with ongoing problems.
Motor Neuron Disease
Amyotrophic Lateral Sclerosis
Motor neurone disease (MND) is a uncommon condition that affects the brain and nerves. It causes weakness that gets worse over time uncommon condition that mainly affects people in their 60s and 70s, but it can affect adults of all ages. “
weakness in your ankle or leg
slurred speech, difficulty swallowing some foods
a weak grip
muscle cramps and twitches
weight loss – your arms or leg muscles may have become thinner over time
difficulty stopping yourself crying or laughing in inappropriate situations” “Usually limb → bulbar → respiratory
- combination of UMN and LMN signs
- LMN = muscle fasciculations, wasting, weakness – main concern
- UMN = increased tone, brisk reflexes
- No sensory involvement
- 10%+ have cognitive decline” “Unique combination of UMN + LMN signs
- EMG - Neurophysiology to confirm muscles denervation, even though can normally been diagnosed in clinic – just to make sure.” “Supportive
- PEG feed, non-invasive ventilation, physio, OT, SALT, care
- Riluzole - delays the onset of ventilator-dependence or tracheostomy in selected patients and may increase survival by approximately two to three months
- Anticipatory / palliative care” “It’s always fatal and can significantly shorten life expectancy, but some people live with it for many years. 3-5 years from symptom onset
- 2-3 years from diagnosis
- 50% die within 14 months of diagnosis
- Bulbar – swallowing etc. that presentation is more aggressive. Die earlier.”
UMN
An upper motor neuron lesion (also known as pyramidal insufficiency) occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. “No wasting - Except from disuse – a little bit of atrophy with long standing disease
- ↑tone (Rigidity – constant stiffness throughout full movement. Spasticity – only through some of the movement – “a catch”)
- ↑reflexes, extensor plantar
- Pyramidal pattern of weakness”
LMN
lower motor neuron lesion is a lesion which affects nerve fibers traveling from the ventral horn or anterior grey column of the spinal cord to the relevant muscle(s) “↓tone
- ↓reflexes, flexor plantar
- weakness”
Brown-Séquard
rare neurological condition hemicord lesion "Contralateral: ↓ pain ↓ temperature" "Ipsilateral: ↓ vibration ↓ joint position sense Weakness"
spinal cord ischaemia
stroke of the spinal cord Atheromatous disease (aortic aneurysm), Thromboembolic disease (endocarditis, AF), Arterial dissection (aortic), Systemic hypotension, Thrombotic haematological disease, Hyperviscosity syndromes, Vasculitis, Venous occlusion, Endovascular procedures, Decompression sickness, Meningovascular syphilis “May have vascular risk factors
- Onset may be sudden or over several hours, Pain, Back pain/radicular, Visceral referred pain, Weakness
- Usually paraparesis rather than quadraparesis given vulnerability of thoracic cord to flow related ischaemia
- Numbness and paraesthesia
- Urinary symptoms
- Retention followed by bladder and bowel incontinence as spinal shock settles” “Don’t always get acute UMN signs.
Might present flaccidly acutely. -Very rarely posterior spinal artery => dorsal columns spared
-Usually anterior spinal artery
-Occlusion of a central sulcal artery can present as a partial Brown-Séquard syndrome
-Usually mid thoracic
-May be spinal shock” MRI- can’t always seen something - go off presentation “Reduce risk of recurrence
-Maintain adequate BP
-Reverse hypovolaemia/arrhythmia
-Antiplatelet therapy
OT and physiotherapy
Manage vascular risk factors” Return of function depends on degree of parenchymal damage, Unless significant motor recovery in first 24 hours chance of major recovery is low. Pain may be persistent and significantly contribute to disability. 20% mortality, only 35-40% have more than minimal recovery
B12 deficiency myelopathy
deficiency can cause degeneration of the lateral and posterior columns normally pernicous anaemia from lack of IF (gastrectomy, crohns, autoimmune, tapeworms) or really bad diet. “Paraesthesia hands and feet, areflexia, First UMN sign extensor plantars,
Painless retention of urine” “Degeneration of:
-corticospinal tracts → paraplegia
-Dorsal columns → sensory ataxia” FBC/blood film (can be neg), B12 “Intramuscular B12 (quicker the better)
If B12 is low normal and low B12 features – treat.” The earlier treated the less likely the they are to be left with a deficit
Spina bifida
Defective closure of the caudal neural tube.
Affects tissues overlying the spinal cord.
Spina bifida = non-fusion of vertebral arches.
Neural tissue may or may not be affected
Spina bifida occulta.
Most minor and common form. Failure of embryonic halves of vertebral arch to grow normally and fuse.
Occurs in lower lumbar vertebrae of 10% of otherwise healthy people.” Usually no clinical symptoms - neural tissue not affected “
May result in dimple with small tuft of hair.” may be incidentally picked up on X-ray
