Neurology Flashcards
Differentiate between CNS & PNS?
CNS = brain & spinal cord, collection of cell bodies = nuclei
PNS = outside the CNS
collection of cell bodies = ganglia
What connects the CNS & PNS?
- 12 cranial nerves - brain & head and neck
- 31 spinal nerves - spinal cord and periphery
the Autonomic nervous system:
- what is it
- where is it
- what are its divisions
- system beyond conscious control, e.g. viscera, smooth muscle, glands, heart
- part in CNS part in PNS
- sympathetic and parasympathetic divisions
What is the sympathetic nervous system
- essentially fight or flight system
- ganglia close to spinal cord
- supply visceral organs and structures of the superficial body organs
Effect of the sympathetic nervous system
- **increases** heart rate & force of constriction in heart
- **vasoconstriction**
- **bronchoDILATION**
- sphincter contract
- decreased gastric secretion & motility
- male ejaculation
Major structure of the sympathetic nervous system?
Sympathetic trunk - two chains of ganglia lying close to spinal cord (one on each side)
Neurotransmitter of sympathetic nervous system and receptor?
Preganglionic: Acetyl-choline ACh to nicotinic receptors
Effector cell: Noradrenaline to adrenergic receptors
What is the parasympathetic nervous system
- essentially the rest and digest system
- some ganglia in brain, some near the organs
Major structure of the sympathetic nervous system?
Cranial nerves 10, 9, 7, 3
Neurotransmitter of sympathetic nervous system and receptor?
Preganglionic: Acetyl-choline ACh to nicotinic receptors
Effector cell: Acetyl-choline ACh to muscarinic receptors
Effect of the sympathetic nervous system
- **decrease** heart rate and force of contraction
- **vasodilation**
- **bronchoCONSTRICTION**
- increased gastric motility and secretion
- spincter relaxation
- male erection
How many pairs of spinal nerves do we have
31 - 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal
Where is the motor cortex located
Precentral gyrus, **frontal lobe**!!
Where is the somatosensory cortex located
Postcentral gyrus, **parietal lobe**!!
Where is the visual cortex located
**Occipital lobe**
Where is the auditory cortex located?
Lateral fissure, **temporal lobe**
What is the frontal lobe responsible for?
higher intellect, personality, mood, social conduct and language (in dominant hemisphere only)
remember by teens - they’ve not developed frontal lobe properly yet lol also pituitary tumour in optic chiasm can cause mood changes
What is the parietal lobe responsible for?
language on dom
sensory perception and integration on nondom
What is the temporal lobe responsible for?
memory and language primary auditory cortex is here!!
What is the occipital lobe responsible for?
vision - primary visual cortex is here!
If a patient has
- recognition deficits (agnosias) - e.g. cannot recognise basic sounds or faces
Where has the cerebrovascular accident occurred?
Temporal lobe
If a patient has
- personality and behavorial changes
- inability to solve problems
Where has the cerebrovascular accident occurred?
Frontal lobe
If a patient has
- visual field defects
and this is a cerebrovascular accident - where has this occurred?
Occipital lobe
If a patient has
- attention deficits, e.g. contralateral hemispatial neglect syndrome (does not pay attention to a side of body)
Where has the cerebrovascular accident occurred and what is the relation to the side of the body neglected?
Parietal lobe
Lesion would be on the opposite of the neglected body side
What is the cerebellum responsible for?
Generally, movement
Which neoplasm causes bitemporal hemianopia?
pituitary adenoma
ah the good old days
What is a dermatome
area of skin supplied by a single spinal nerve
What is a myotome
muscles supplied by a single spinal nerve
Name cranial nerves in order!!
(mnemonic & names)
Oh Oh Oh They Traveled And Found Voldemort Guarding Very Ancient Horcruxes.
Olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal
Nerves for sensory, motor or both?
(mnemonic)
Some say money matters but my brother says big brains matter most
Parasympathetic nerves?
(mnemonic & which)
1973
10 - vagus
9 - glossopharyngeal
7 - facial
3 - oculomotor
Nerves of the eye?
(mnemonic & what they stand for)
SO4 LR6 3
How would you interpret the results of CN I tests
If **anosmia**: causes are
- meningioma
- trauma - skull or cribriform plate
- Parkinson’s
- mucus block / covid / genetics
How would you test CN II
visual acuity
- distance - Snellen chart & pinhole
- colour vision - ishihara plates
fields
- neglect / inattention
- field - formal is **Amsler chart**
- blind spot
optic disc
- fundoscopy
Pupil
- pupillary light reflex (direct - ipslateral, consensual - contralateral, swing check relative afferent pupillary defect)
- accomodation reflex - distant to near
- size, shape
Visual field defects - key in investigation?
Test one eye while covering the other! Patient often do not realise
**bitemporal hemianopia**
- what is it?
- pathology?
- loss of temporal visual field in both eyes
- optic chiasm tumour
**Homonymous field defects**
- types
- pathology?
- hemianopias or quadrantanopias
- same side of visual field in each eye
- pathology is behind optic chiasm in visual pathways: stroke, tumour, abscess
**Scotoma**
- what is it?
- pathology?
- absent or reduced vision surrounded by areas of possible vision
- wide range, including demyelinating (MS, DM)
**Monocular vision loss**
- what is it?
- pathology?
- total loss of vision in one eye secondary to optic nerve pathology or ocular disease
How would you interpret results of a fundoscope exam?
if papilloedema, causes are
- usually **ischaemia** - intracranial bleed possible
- **hypertension** - systemic, intracranial (benign & malignant → suspect a brain tumour!)
- **headache**
- **brain tumour** causing compression
- prolonged CNS infection
Nerves of the eye again!!
(mnemonic & what they stand for)
SO4 LR6 3
Strabismus
- what is it?
- pathology?
- how would you assess it?
- condition where eyes do not properly align with each other when looking at an object
- pathology affecting III, IV & Vi (and/or) can all cause strabismus
- test by corneal reflex test / Hirschberg test and or cover test
How would you test CN VII?
By facial expressions:
- raising eyebrows
- closing eyes
- blowing out cheeks
- smiling
- pursing lips
How to differentiate between a Facial Palsy and a stroke?
stroke is forehead sparing whereas the nerve palsy is not!!
Differentiate between Bell’s palsy and facial palsy?
Facial palsy is termed Bell’s palsy when it is idiopathic
Define stroke?
neurological deficit lasting longer than 24 hours due to vascular compromise
What are ischaemic strokes? Subclassify?
Reduction in cerebral blood flow due to arterial occlusion or stenosis
= anterior / middle / posterior cerebral artery / lacunar
(thrombotic / embolic)
How can you distinguish haemorrhagic and ischaemic strokes?
No reliable way
tho intracerebral more often associated with severe headaches or coma → ICP ++
patients on anticoag: assumed to have haemorrhage unless proven otherwise
Associated risk factors for ischaemic strokes?
AF - higher risk of thrombus / embolus
atherosclerosis
shock
vasculitis
What are haemorrhagic strokes? Classify?
Ruptured blood vessels leading to reduced blood flow
Intracerebral / subarachnoid / intraventricular
Risk factors for strokes?
Hypertension, age, AF
Smoking, diabetes, hypercholesterolaemia, polycythaemia
medications - HRT, combined oral contraceptive pill
FAST tool to identify stroke in community?
Face, Arm, Speech, Time
Tool used to identify strokes in ER?
ROSIER
Differentiate stroke from bell’s palsy?
Stroke = forehead sparing = Upper motor neuron lesion
Bell’s palsy = everything on face = Lower motor neuron lesion
Investigations for Stroke?
Head CT
→ rule out haemorrhagic before thrombolysis & LP
→ aspirin 300mg stat post CT
LP - MUST if CT normal
not before 12h - xanthochromia
Pulse, BP, ECG
look for AF / if high BP then must maintain!! 20% will compromise cerebral perfusion
Bloods
thrombocytopenia & polycythaemia - rule out hypoglycaemia
3 layers of meninges of the brain?
IN → out
Pia mater, arachnoid mater, dura mater
Risk factors for an extradural haemorrhage?
Young patient with traumatic head injury + ongoing headache
periods of improval then rapid decline (haematoma getting larger to compress intracranial contents)
How might an extradural haemorrhage appear on CT?
Lentil / lemon, biconvex
Limited by cranial sutures!
How might a subdural haemorrhage appear on CT?
Crescent
Not restricted by suture lines!
Risk of subdural haemorrhage?
elderly, alcoholic patients
→ atrophy in brian = more likely to rupture
How might an subarachnoid haemorrhage appear on CT?
Star / around the brain
Causes of subarachnoid haemorrhage?
Usually ruptured cerebral aneurysm
= berry aneurysm = 80%
arterio-venous malformations
others: enceph, vasculitis, tumour, idiopathic
Risk for subarachnoid haemorrhage?
Hypertension, smoking, excessive alcohol consumption, cocaine
sickle cell anaemia
fam hx, also black female 45-70
Symptoms of a subarachnoid haemorrhage?
Sudden and severe thunderclap headache hitting on the back of the head
→ Most severe at beginning, short period
N+V, collapse, seizure
can present with meningism
How should you treat haemorrhagic strokes (4)?
Do not give antiplatelets!!
Reverse anticoagulants
Control hypertension
Nimodeipine
Decompression of raised ICP
Mannitol (diuretic) / Burr holes
What is nimodepine?
a CCB
Prevent & tx of ischaemic neurological defects following aneurysmal subarachnoid haemorrhage
How might you reverse warfarin?
Human Prothrombin Complex (Beriplex) & Vitamin K
if unavailable - fresh frozen plasma
Direct Oral anticoagulants (DOAC) reversal:
Agents for Dabigatran, rivaroxaban, apixaban?
Dabigatran = Idarucizumab
Rivaroxaban & Apixaban = Andexanet alfa
(R&A = direct factor Xa inhibitor)
(D = direct oral anticoag)
Surgical interventions for intracranial bleeds?
Coiling - place platinum coils into aneurysm and seal it off from artery
Clipping
→ not indicated unless ruptured
Complications of intracranial haemorrhages?
Vasospasm - can result in brain ischaema
Hydrocephalus - buildup of fluid in ventricles
(LP or shunt)
Seizures
(prevent with nimodipine)
Features of anterior cerebral artery stroke?
Limb dysfunctions
gait apraxia, truncal ataxia, incontinence
**Sensory loss, mostly in lower limbs** amarosis fugax (transient vision loss)
Features of middle cerebral artery stroke?
Upper limbs > lower limbs
Facial / speech features
facial droop, aphasia
homonymous hemianopia
hemineglect in non dominant hemisphere
Features of posterior cerebral artery stroke?
Heavy visual features
visual agnosia - cannot interpret info but can see
colour naming / discriminating problems
double vision, visual field defects
contralateral homonymous hemianopia w/ macular sparing
(loss sight same side both eyes)
Features of a lacunar stroke?
lacks true cortical signs: aphasia, visuospatial neglect, gaze deviation, visual field defects
Involves limbs more than head
pure sensory impairment / motor stroke, ataxic hemiparesis (weak in leg), clumsy hand etc
Treatment principles, ischaemic stroke?
Thrombolysis = up to 4.5 hours since onset of symptoms
Thrombecttomy = 6-24 hours since onset
Clopidogrel 24 hours after both
if both unsuitable: aspirin daily 2weeks then lifelong clopidogrel
What is thrombolysis?
give within 4.5 hours of onset
ischaemic stroke
→ once excluded primary ICH with CT!
Alteplase = tissue plasminogen activator, breaksdown clots & reverse stroke
Monitor for complications e.g. IC / systemic haemorrhage = repeat CT
What is thrombectomy?
= mechanical removal of clot
give 6-24 hours since onset of symptoms
→ must confirm occlusion on imagine
→ clopidogrel 24 hours after
How might you prevent stroke?
Platelet tx
Clopidogrel 75mg daily ± aspirin
(alt dipyridamole)
Cholesterol treatment
atorvastatin 80mg
(alt simvastatin)
Tx modifiable risk factos
AF = warfarin / DOAC
BP - ACEi
Mechanism of statins?
Inhibit HMG-CoA, thereby decreasing production of LDL levels
Define transient ischaemic attack?
neurological deficit lasting less than (or up to) 24 hours
Management for TIA’s?
If on anticoag → immediate admission
aspirin 300 mg stat
daily until specialist review
What is epilepsy?
a recurrent tendency to have spontaneous, intermittent, abnormal electrical activity in parts of the brain, manifesting in seizures
What is a seizure?
transient episodes of abnormal electrical activity in the brain as caused by excessive, hypersynchronous neural discharge
Diagnostic criteria, epilepsy?
= at least 2 or more unprovoked seizures occurring > 24hrs apart to DIAGNOSE EPILEPSY
What is syncope? Risk factors?
= loss of consciousness due to hypoperfusion to brain
Risk - prolonged upright position, sweating, nausea, issues w/ heart / BP etc
Differentiate non-epileptic seizures to epileptic seizures?
Non epileptic = situational, situational, with pre-ictal anxiety
Epileptic = result from sleep, can have incontinence & sleep
General advice for patients with epilepsy?
→ CANNOT DRIVE = inform DVLA
until free of day time seizures for minimum a year
→ try not to swim alone, avoid dangerous sports, leave door open when taking bath
Causes of epilepsy?
⅔rd idiopathic, often familial
Post CNS infection → cortical scarring ‘sclerosis’
Space occupying lesion, stroke, alzheimer’s / dementia, alcohol withdrawal
Risk factors for epilepsy?
Fam hx
Premature born babies
Abnormal blood vessel in brain
arterio-venous malformations
Use of drugs - cocaine
Alzheimer’s / dementia
stroke / brain tumour / infection
DIfferentials for epilepsy?
Syncope = most common
- *Dissociative (non-epileptic) seizures**
- situational, durational, dissociative
- eyes closed, can cry / speak, same f but larger amp
Investigations & Diagnosis for epilepsy?
> 2 seizures 24 hours apart
→ diagnosis of exclusion
EEG (checks for which type)
MRI brain (structural problems / tumours)
CT head - space occup lesion
exclusions - ECG for heart
4 stages of epileptic attacks?
Prodrome = change of mood or behaviour
aura = deja vu, strange feeling in gut, flashing light
ictus = the seizure, 30-120s
Post-ictally = after seizure
Examples of post-ictally behaviour?
Amnesia
Headache, confusion, myalgia and sore tongue (might be bitten)
Temporary weakness after focal seizure in motor cortex = todd’s palsy
dysphagia following temporal lobe seizure
What are generalised seizures?
Bilateral, symmetrical & synchronous motor manifestations
What are focal seizures?
Features referable to one part of a hemisphere
Floaters in vision field / visual flashes
Which lobe can the seizure be located to?
Occipital lobe
= visual
Pins and needles, pricking, ants are crawling over skin
Which lobe can the seizure be located to?
Parietal lob
= sensory seizures
Hallucinations, lip smacking / grabbing, plucking, sense of deja vu
Which lobe can the seizure be located to? Feature post-ictally?
Temporal lobe
Post ictally = dysphagia
Head / leg movements, posturing, start from one point then → whole body
Which lobe can the seizure be located to? Post-ictally features?
Frontal lobe
= motor
- *Post ictally = weakness**
assoc. Todd’s palsy = paralysis of limbs involved for hours
What is status epilepticus? How would you manage it?
→ seizures lasting > 5 minutes or > 3 seizures in one hour
= medical emergency
IV lorazepam 4mg, repeat aft 10 minutes if seizure continues
If still = IV phenobarbital or IV phenytoin
Other options
buccal midazolam, rectal diazepam
What are Tonic-clonic seizures?
tonic = muscle tensing clonic = muscle jerking
What are absent seizures?
→ typically in children
blank, stares into space and abruptly returns to normal
often don’t realise, 10-20s,
> 90% grow out of it
Feature of absent seizure on EEG?
3Hz spike and wave activity!
What are atonic seizures?
Drop attacks = sudden loss of muscle tone and cessation of movement = fall
typically > 3 minutes, begin in childhood
differential is lennox-gastaut syndrome
What are myoclonic seizures?
→ usually in children, as a part of juvenile myoclonic epilepsy
sudden brief muscle contractions, like a sudden ‘jump‘
= a violently disobedient limb or be suddenly thrown to the ground
If a child presents with myoclonic seizure, test you should do?
Genetic testing
Treatment principles for epilepsy?
For generalised seizures
→ 1st = sodium valproate
→ 2nd = lamotrigine or carbamazepine
Reverse for focal seizures
Sodium valproate
Class / mechanism / SE / CI?
antiepileptics
increase GABA activity → relax the brain
SE = teratogenic, liver damage & hepatitis, hair loss, tremor
CI = girls & women of reproductive age!
Carbamazepine
Class / Mechanism / SE?
antiepileptic
Inhibit neuronal sodium channels
SE - agranulocytosis (carbimazole also)/ aplastic anaemia / CYP450
(also for trigeminal neuralgia)
Lamotrigine
class / SE
antiepileptic
also for bipolar disorder
SE Stevens-Johnson syndrome / DREE = life threatening rashes!!
+ leukopenia
Surgical options to treat seizures?
Surgical resection = if single defined cause or area
Vagal nerve stimulation / disconnection
What are infantile spams?
West syndrome, rare
start around 6m infancy, clusters of full body spasms
Treatment for infantile spams?
1st line prednisolone & vigabatrin
What is Parkinson’s?
Degeneration of the pars compacta in substantia nigra of brain leading to decrease in dopamine
Causes & risk factors of Parkinson’s
No known cause
Genetic mutations - PINK1, Parkin etc
Risk
Pesticide exposure, MPTP in illegal opioids
male, age, fam history
! non smoker = higher !
Presentation of Parkinson’s?
TRAP
+ sleep disturbances / anosmia
T = tremor = resting!
pill rolling tremor
R = rigidity
cogwheel rigidity, esp in arms
A = akinesia / dyskinesia
reduced arm swing, shuffling gait, soft voice, reduced blinking, drooling
P = postural instability
& forward tilting
→ NO WEAKNESS
Differentials for Parkinson?
Benign essential tremor
Dementia with lewy bodies
Progressive suprenuclear palsy
if on Levodopa
high response = lewy body dementia
(hallucinations, agitation, confusion)
low response = Multi-system atrophy
(symmetrical, worse on mvt, no other parkinson features, better with alcohol)
Investigations for Parkinson’s?
CT / MRI
PET with fluorodopa
localises dopamine deficiency in basal ganglia
What might you find on an autopsy of a Parkinson patient?
Lewy body depositions = eosinophilic protein aggregations in substantia nigra, cytoplasm rich in eosin
disappearance / fading of the substantia nigra
Most effective tx for Parkinson’s?
Levodopa = 1st line
if motor symptoms not affecting patient’s QoL then others or levodopa
Levodopa
class / mechanism / SE
synthetic dopamine (precursor)
→ boost patient’s dopamine level
→ give with COMT
SE less effective over time, if dose too high = dyskinesia (N+V, arrhyth, chorea, dystonia)
COMT inhibitors
Examples / Mechanism?
entacapone, tolcapone
Inhibition of breakdown of dopamine by Catechol-O-Methyl Transferase enzymes
used in conjunction w/ levodopa
Dopamine Receptor Agonists
Examples / mechanism / SE
bromocriptine / cabergoline
= stimulate dopamine receptors
SE impulse control disorders, hallucinations, excessive daytime somnolence
MAO-B inhibitors
Examples? Mechanism?
Selegiline, rasagiline
Inhibits breakdown of dopamine by Monoamine oxidase-B enzymes
Surgical tx options for Parkinson’s?
Deep brain stimulation
Define dementia?
Clinical syndrome characterised by significant deterioration in cognitive skills → impairment of normal function
Reversible causes of dementia & tx (5)?
aka differentials of dementia?
alcohol
hypothyroidism (THR)
vitamin B12 deficiency
Syphilis (penicillin)
Normal pressure hydrocephalus
(ventriculoperitoneal shunt)
What is an Normal pressure hydrocephalus?
= abnormal venous drainage of cerebrospinal bluid → backup of fluid & hydrocephalus
symptoms = dementia, urinary incontinence, magnetic gait
MRI - no cortical atrophy, ventriculomegaly of all ventricles, patent cerebral aqueduct
Tx ventriculoperitoneal shunt
Irreversible causes of dementia? (Types of dementia)?
Alzheimer’s disease
Vascular dementia
Lewy body dementia
Frontotemporal dementia
Briefly outline pathophysio of Alzheimer’s?
neurofibrillary tangles & beta amyloid plaques affect function of neurons → interrupt key neuron process → cell death
What can be found on a brain biopsy in someone with Alzheimer’s?
Neurofibrillary tangles (tau protein aggregations) & beta amyloid plaques
Widespread cerebral atrophy esp. cortex & hippocampus
Key presentation of Alzheimer’s?
Memory loss
Loss of personality, intellect & language
Investigations for Alzheimer’s?
= Exclude
CT / MRI → hippocampus & cortex atrophy
definitive is actually brain biopsy but obv impossible until death
Treatment option for Alzheimer’s?
Symptomatic
Cholinesterase inhibitors
(+ACh levels)
NMDA receptor antagonists
Depression = SSRI
Key presentation vascular dementia?
Step wise steady & gradual deterioration related to region (and a history) of stroke / TIAs
Symptoms of vascular dementia?
Urinary incontinence, cranial nerve palsy, focal neurological deficits
Treatment for vascular dementia?
None to reverse
→ Prevent another stroke
= BP, lifestyle, smoke, antiplatelet = aspirin
(nimodepine is ischaemic)
Key presentation frontotemporal dementia?
< 65 years
Personality change, lack of social inhibition
What might you find on an imaging scan of frontotemporal demential patient?
Atrophy of frontal & temporal lobes
sparing other lobes!
Treatment for frontotemporal dementia?
No tx available to delay progression
SSRI = behavoural symptoms
(setraline, citalopram)
Atypical antipsychotics = psychosis
Symptoms of Parkinson’s disease & lewy body dementia?
- *= Parkinsonism**
- *= TRAP**
Tremor (resting)
Rigidity (esp in arms)
Akinesia / bradykinesia
Postural instability
Differentiate Parkinson’s disease dementia x Lewy body dementia?
→ sequence of events
Parkinson’s = Parkinsonism THEN dementia
Lewy body = dementia THEN Parkinson
If on Levodopa, how might you differentiate Lewy body dementia x Parkinson’s disease dementia?
Responds well = Parkinson’s d.d.
If 3 tions: hallucination, agitation & confusion → Lewy body dementia as patients are dopamine sensitive
Other features of lewy body dementia?
Recurrent visual hallucinations
Flunctuating attention / alertness / cognition
Sleep disturbances
Tx for Lewy body dementia?
Cholinesterase inhibitors = improve symptoms, but don’t slow progression
Levodopa = helps with motor impairment but risk of developing delirium
→ CI antipsychotics (worsen!)
What is Huntington’s disease?
Autosomal dominant
genetic condition, progressive deterioration in the nervous system
Genetic stuff for Huntington’s?
Trinucleoside repeat disorder = CAG
Genetic mutation on HTT gene on chromosome 4
What is anticipation?
= in Huntington’s
each successive generation have more repeats in gene
= earlier age of onset
= increased severity of disease
Presentation - Hungtington’s?
30-50 years, but can be earlier or later
Chorea
= involuntary, purposeless movements
= parakinesia = try to incorporate into purposeful mvt
Dementia
= cognitive decline
Behavior changes
= cognitive, psychiatric, mood problems,
dysarthria / dysphagia / dystonia + parkinson’s
How might you diagnose Hungtington’s chorea?
blood PCR for CAG repeats
MRI = atrophy of caudate & putamen, enlargement of the lateral ventricles
Tx for Hungtington’s?
No tx for slow or stop
Symptomatic relief / MDT in QoL
speech & language / genetic counselling / advanced directives
chorea = antipsychotics, benzodiazepine
Prognosis for Huntington’s?
Progressive condition
LE 15-20 years after onset
death often due to respiratory, e.g. pneumonia, but also common is suicide 😞
Before any headache investigation - one thing to rule out?
Idiopathic cranial hypertension
Signs of raised intracranial pressure?
headache, vomitting, reduced levels of consciousness, papilloedema
Cushing’s triad
widening pulse pressure, bradycardia, irregular breathing
Presentation & risk - idiopathic intracranial hypertension
headache, blurred vision, enlarged blind spot, papilloedema, ± 6th nerve palsy
risk → obesity, female, pregnancy, drugs (COCP, steroids, tetracyclines, lithium)
Signs of papilloedema?
Optic nerve swelling & blurring of the disc margins
cotton wool spots, silver wiring,
hard exudates, retinal haemorrhage
→ seen on a fundoscope
Tx Idiopathic intracranial hypertension?
1st line = Weight loss
Diuretics = acetazolamide
Topiramate (anticonvulsant) = also cause weight loss
Surgery
optic nerve sheath decompression and fenestration
Thunderclap headache?
Subarachnoid haemorrhage!
Thunderclap headache?
Subarachnoid haemorrhage!
Presentation of tension headaches?
Aches across the forehead in a band pattern
Pressing & tightening
come and go
no N&V
Tx Tension headaches?
- *Basic analgesia**
- *= aspirin / paracet / ibuprofen**
Consider amitriptyline
Relaxation techniques & hot towels to local area
Tension headache associations
stress / depression / alcohol / skipping meals / dehydration
Triggers of migraines?
= chocolate
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie in’s
Alcohol
Tumult - loud noise
Exercise
Risk factors for migraines?
females, positive family history
Presentation of migraine?
moderate to severe intensity
- *pounding or throbbing in nature**
- *nausea & vomiting**
± aura
± photophobia, phonophobia
What is aura & examples?
prodrome / postdrome to migraine
visual = flashing light, zigzag lines, lose part of vision, black holes in visual field
sensory = parasthesia
speech or language = problems saying / understanding words
Diagnostic criteria for migraines
5 attacks
Acute management for migraines?
oral triptan ± paracetamol
or other analgestics = aspirin / paracetamol
Preventive management for migraines?
Topiramate / propanolol
→ amitriptyline
→ 10 sessions of acupuncture over 5-8 weeks
- *Riboflavin** (vit B12)
- *Botulinum Toxin type A** = last line
(CI teratogenic / asthma)
Presentation of cluster headaches?
→ headache + unilateral,
ipslateral eye concentrated
red, swollen, watering eye
miosis = constrict, ptosis = eyelid droop
nasal discharge, facial sweating
→ 5 to diagnose
→ episodic, can wake pt
Triggers of cluster headaches?
Alcohol, strong smells, exercise
Acute treatment for cluster headaches?
100% 15L O2
15-20 minutes via non-rebreathable mask
CI if COPD
Triptan = SC sumatriptan 6mg
→ serotonin receptor agonist = reduce vascular inflammation
Preventive measures for cluster headaches?
1st line CCB = verapamil
Avoid alcohol during cluster period
Corticosteroids may help during cluster period (prednisolone short course 2-3 weeks to break cluster)
Presentation - trigeminal neuralgia?
Intense facial pain, similar to electric shock / shooting pain lasting seconds to minutes
related to eating
Branches of the trigeminal nerve?
Ophthalmic (v1)
Maxillary (V2)
Mandibular (V3)
→ any combination can be affected)
Tx trigeminal neuralgia?
1st = oral carbamazepine
2nd oral phenytoin, gabapentin & lamotrigine
Surgical - microvascular decompression / gamma knife surgery
(anticonvulsants)
Associations & triggers - trigeminal neuralgia?
5-10% multiple sclerosis
triggers: cold weather, spicy food, caffeine, citrus fruits, brushing teeth, cough / sneeze
Medication overuse headache - diagnostic criteria? triggers?
Headache present ≥ 15 days / month
Triggers = opioids, triptanss, combination analgesic (paracetamol + codeine / opiates)
Present sinusitis?
Headache associated with inflammation of sinuses
→ if tender over the sinus = DIAGNOSTIC
facial pain behind nose, forehead and eyes
Treatment sinusitis?
Resolve in 2-3 weeks, mostly viral
tx
- *nasal irrigation with saline**
- *prolonged = steroids nasal spray**
Cervical spondylosis - present & diagnose?
Degenerative changes in cervical spine = diag by exclusions
Neck pain worsened by mvt
Hormonal headache - present & tx?
related to low oestrogen, nonspecific tension like headache
→ 2 days before & first 3 days of menstruation, menopause, pregnancy
= 2 out of 3 menstrual cycles for diagnosis → headache diary
What is Horner’s syndrome?
- *ptosis, miosis, anhydrosis**
- *→ all on the same side**
flushing on one side of the face and that side doesn’t sweat. The eye on the same side has a smaller (constricted) pupil with a drooping or weak eyelid.
Define meningitis?
inflammation of meninges
What is meningism?
Neck stiffness / photophobia /
Kernig’s sign
= pain & resistance on passive knee extensions with hips fully extended
Presentation - meningitis?
triad
Fever, headache, neck stiffness / leg pains
N + V, photophobia, rash (non blanching)
Causes of meningitis?
Bacterial / viral / fungal / parasitic
How might you treat primary meningitis?
IV / IM Benzylpenicillin
or IM ceftriaxone
Secondary tx for meningitis?
GCS assessment
Blood cultures + broad spectrum antibiotics
Steroids
= IV dexamethasone to reduce tissue inflammation, damage & reduce morbid
usually - CT before LP
DIAGNOSTIC = Lumbar puncture
CI: coagulation disorders, rash, raised intracranial pressure
Initial antibiotics for meningitis? Any to add?
Ceftriaxone or cefotaxime
if allergy = (erythro?)
if immunocompromised + amoxicillin
(risk of listeria)
if travel hx + vancomycin
(risk of penicillin resistance)
If there is a rash - most likely causative organism? special response?
Rash = most likely
neisseria meningitidis
→ inform PHE
→ identify close contacts: prophylactic antibiotics = ciprofloxacin / rifampicin
Causative bacteria for meningitis? (6+2)
GRAM NEG
Neisseria meningitidis
E coli
Haemophilius influenza B
GRAM POS
Listeria spp.
Strep pneumoniae
Group B strep.
Chronic
Mycobacterium Tuberculosis
Syphilis
Meningitis in - neonates, pregnant ladies, immunosuppressed patients, elderly
Listeria spp.
Causes of meningitis in adults (2)?
Neisseria meningitidis
Strep pneumoniae
Viral causes of meningitis?
Herpes Simplex (HSV) Varicella Zoster (VZV) Enterovirus
Fungal causes of meningitis?
Cryptococcal spp.
Cause of meningitis when LP / CSF is
‘fibrin web’ appearance
high WBC = lymphocytes
high protein
low glucose
Fungal / TB
→ PCR for M. TB
Cause of meningitis when LP / CSF is
cloudy
high WBC = neutrophil / granulocytes
high protein
low glucose
Bacterial
Cause of meningitis when LP / CSF is
clear
high WBC = lymphocytes
high protein
normal glucose
Viral
PCR for HSV, VZV & enterovirus
How might you test for TB?
Phenol auramine / Ziehl-Neelson stain
Differentiate between TB / bacterial causes of meningitis as appeared on CSF?
Bacterial = neutrophils / other granulocytes
TB / fungal = neutrophils = lymphocytes
Differentiate between TB / fungal and viral caused meningitis as appeared on CSF?
viral = glucose normal
TB / fungal = high glucose
Signs of sepsis?
= prolonged refill time
cold hands and feet
decreasing BP
evolving rash
Sepsis 6 tx?
Give
oxygen
fluid resuscitation
IV antibiotics
Take
Blood cultures
Urine putput
Lactate
What is encephalitis?
Inflammation of the cerebral cortex
= severe abnormalities in function of brain
Causes of encephalitis?
(name essential at least)
usually Viral
→ Herpes Simplex virus
→ Varicella zoster virus
MMR, EBV, HIV if immunocompromised, CMV, Coxsackie
- *Tropical**
- *mozzie bite**: Japanese encephalitis / West Nile
- *animals**: tick borne / rabies
Present - encephalitis?
acute flu-like illness, hours to days
fevers, seizures
altered GCS - confusion, agitation, drowsiness, coma
- *± meningism**, mostly absent
- *check travel tx / animal bite**
Investigations / initial management encephalitis?
IV Acyclovir
Contrast enhanced CT
must preceed LP
Lumbar Puncture
high lymphocytes
high protein
normal glucose
viral PCR
(throat swab & MSU)
blood culture, toxoplasma IgM titre, malaria film, gram film → negative
Treatment for encephalitis?
if HSV or VZV = acyclovir
PCR at the end of cycle
others mostly supportive
→ lots of neuro rehab
Cause of tetanus?
Clostridium tetani
gram pos rod, anaerobic spore
in soil & house dust
inoculation through skin
TETANUS CARDS
RABIES CARDS
CJD CARDS
What is Guillan Barre syndrome?
Acute, inflammatory polyneuropathy
→ ascending neuropathy resulting in weakness & reduced reflexes
Risk factors for Guillan Barre syndrome?
peak 15- 35, 50-75
males > females
after pregnancy (delivery)
Causes of Guillan Barre?
History of preceeding illness
Diarrhea or a respiratory illness
→ Campylobacter jejuni = most common
→ causes gastroenteritis
Viral causes
Cytomegalovirus (CMV), Epstein Barr, Zika, HIV
Post vaccinations
Pathophysio - Guillan Barre?
Immune mediated damage to peripheral nerves
= molecular mimicry
= antibodies generated in response to pathogen incorrectly cross react with body’s own cells
Presentation - Guillan Barre?
Prodrome = usually gastroenteritis & flu like illness
Ascending neuropathy = symmetrical
feet → facial / respiratory
→ reduced reflexes
→ weakness
→ peripheral neuropathy
→ loss of sensation
What is Miller Fisher syndrome?
Variant of Guillan Barre
= ataxia, areflexia, ophthalmoplegia
with anti-GQ1B antibodies
(component of nerves)
Differentials for Guillan Barre?
Lyme disease
sarcoidosis
Thiamine deficiency
Neoplasms
Investigations for Guillan Barre?
DIAGNOSTiC = Nerve conduction studies
= reduced signal through nerve, prolonged distal motor latency ± conduction block
Lumbar puncture at L4
high protein, normal cell count, normal glucose
Spirometry = monitor FVC
decrease FVC = admit to ITU for maintenance of airways
Bloods → check for IgA deficiency, if yes cannot tx IV IG = severe allergic reaction
Treatment of Guillan Barre?
Plasmaphoresis
IV Immunoglobulin
CI: IgA deficient patients → anaphylaxis!
(plasma exchange)
Complications of Guillan Barre?
Respiratory failure, infection, cardio dysfunction & pulm embolism
→ monitor BP, FVC, low limb stockings & LMWH prophylaxis for venous thrombosis
Tx neuropathic pain?
gabapentin / carbamazepine
(anticonvulsants)
Criteria for assessment for tx pathways, Guillan Barre?
Hughes Disability score
What is myasthenia gravis?
Neuromuscular autoimmune disorder, due to antibody mediated blockage of neuromuscular transmission
Risk & aetiology, myasthenia gravis?
20-30’s females
60-70’s males
Pathophysio of myasthenia gravis?
Acetylcholine receptor antibodies (ACH`r-Ab / anti ACh) binds to ACh receptors at neuromuscular junction
= prevents binding of ACh & subsequent depolarisation needed for muscle contraction
AChR-Ab
produced by? ways it affects NMJ?
produced by B lymphocytes
prevents binding by ACh
cross link ACh-R = internalisation & destruction
Complement mediated damage of post synaptic membrane
What type of hypersensitivity reaction is myasthenia gravis?
antibody mediated = type II
Other antibodies in Myasthenia Gravis?
AChR-Ab = 80-90%
anti MuSK protein
anti LRP protein
Associations - Myasthenia Gravis?
Thymus abnormalities
85% hyperplasia, 15% thymoma
autoimmune associations
Grave’s SLE, rheum art
Transient MG - caused by D-Penicillamine treatment for Wilson’s disease
Clinical presentation - Myasthenia Gravis
hallmark = fatiguability of muscles
increasing weakness with use
→ common at the end of the day or following exercise
Signs by region
Limbs = arms > legs
can’t hang up laundry / comb in one go
Myasthenic sneer = facial muscles
expressionless, poor smile
dropped head at the end of day
bulbar = count to 50 = voice smaller
ophthalmic
Investigations for myasthenia gravis?
Ice pack test
ptosis improve after application of ice
(neuromuscular transmission better at lower muscle temp)
Cogan’s lid twitch
patient to follow pen down … and suddenly up = lid will overshoot and twitch
Bloods for AChR-Ab, MuSK & LRP4
if negative = Electromyography (90% sensitivity)
Thymus assessment (CT chest)
+ thyroid function test (highly assoc)
Pharmacological treatment (with class) for myasthemia gravis?
1st = pyridostigmine
2nd = Prednisolone
corticosteroids
3rd = immunosuppressants
azathioprine = inhibit purine synthesis
risk of marrow failure
Class of pyridostigmine? Mechanism? SE?
Acetylcholinesterase Inhibitors
prevent hydrolysis or acetylcholine and increase effect at NMJ
SE cholinergic = secretions, diarrhoea, GI upset, bronchospasm, sweating, urinary incontinence
→ avoid during acute myasthenic crisis
Other management options, myasthenia gravis?
FVC manage, speech and language team
IV Immunoglobulin
if severe respiratory or bulbar symptoms
alt plasmaphoresis
Thymectomy for thymomas
High dose steroids if ventilated
initially worsen then better
What is a myasthenic crisis?
Worsening weakness that requires respiratory support, e.g. intubation / ventilation
Presentation - myasthenic crisis?
Severe limb weakness, diplopia
Hypoxia
quiet breathing, reduced chest expansion, tachy, HP
sats & ABG can be normal
Tx myasthenic crisis?
Urgent admission to hospital
intubation / non invasive ventilation
FVC / single breath count = BEST investigate !!!
all to be assessed by speech & language team & regularly FVC assess
What is Lambert Eaton syndrome?
Antibodies against voltage gated calcium channels on presynaptic junction
ACh release reduced = muscle weakness
Causes of Lambert Eaton syndrome?
Autoimmune related
both MNJ & autonomic ganglia
90% seropositive
50-60% have underlying malignancy
small cell lung CA, lymphoproliferative
STRONG relate w/ T1DM, Thyroid diseases
Presentation Lambert Eaton syndrome?
hallmark = strength increases with repeated effort / exercise!
Proximal muscle weakness
→ in the morning
dry eyes, dry mouth, sexual dysfunction, sphincter issues, postural hypotension
Management - Lambert Eaton syndrome?
ACh inhibitor = pyridostigmine
(goes both ways_
3, 4 diaminopyridine = blocks K channel in nerve terminal & potentiates action
treat cancer / use steoids may also help
What is Isaac’s syndrome?
Peripheral nerve hyperexcitability due to antibodies against voltage gated potassium channels
cramps, fasciculations, hyperhydrosis, myokymia, exercise intolerance
What is Multiple Sclerosis?
Chronic progressive condition that involves demyelination of the myelinated neurones in the CNS
Causes & risk of Multiple Sclerosis?
Autoimmune = T cell mediated
20-40’s, women!!!
Others
genetics / Epstein Barr virus / low sun or vit D / smoking & obesity
What are myelins? Produced by which cells?
Myelin = sheath of the axons of neurones in CNS
→ produced by oligodendrocytes = affected in MS
Pathophysio of multiple sclerosis?
Inflammation around myelin & infiltration of immune cells = damage to myelin
Plaques of demyelination occur around veins (perivenular) & have a predilection for distinct CNS sites:
optic nerves, ventricles of brain, corpus callosum, brainstem & cerebellar connections etc
Type of reaction for Multiple Sclerosis?
Type 4 = cell mediated hypersensitivity
(T cells / B cells / macrophages)
Symptoms of Multiple Sclerosis?
Charcot’s neurologic triad +3
Dysarthria = plaques in brainstem
speech / eat / swallow / talk = throat
Intention tremor = plaques in motor pathways
limb weakness & spasms, tremors, ataxia
Nystagmus = plaques in eye nerves
optic neuritis, diplopia
loss of vision / pain
Paraesthesia = plaques in sensory pathways
Lhermitte’s sign
electric shock runs down back & radiate to limbs when bending neck
Plaques in ANS
Incontinence / sexual dysfunc / bowel symptoms
Mneumonic for Multiple Sclerosis symptoms?
LOVDIP
Lhermitte’s sign, limb weakness
Optic neuritis
Vertigo
Diplopia
Incontinence
Paraesthesia
Immediate treatment with optic neuritis?
seen urgently by ophathalmologist
Steroid treatment, 2-6 weeks recovery
What are the four disease patterns of multiple sclerosis? Briefly describe each one? Which is the most common?
Replasing / remitting MS (80%)
no increase in disability between bouts months apart
Secondary progressive MS
over time from RRMS disability progression becomes constant
Primary Progressive MS
steady disability progression
Progressive relapsing MS
steady disability + bouts superimposed
Differentials for MS?
SLE
Parkinson’s
Motor neurone disease
Diagnostic criteria & investigations?
Criteria = 2 or more attacks disseminated in time & space (affecting diff parts of CNS)
DIAGNOSTIC = MRI
90%+ white matter plaques
Lumbar puncture = CSF shows IgG bands (antibodies)
Electrophysiology = visual evoked potential studies → delayed conduction = demyelination
How might you differentiate between active & chronic lesions of MS?
use Gadolinium contrast in MRI
Lesions that are enhancing = break in BBB & uptake gd = active
Not enhancing = old
Current pharmacological treatment for MS?
→ disease modifying = induce remission with no evidence of disease activity
Monoclonal antibodies = IV alemtuzumab, natalizumab
dimethyl fumarate
How might you treat an acute MS attack?
steroids = oral methylprednisolone 500mg daily for 5 days / IV 1g / day if severe
if frequent relapses = anti-inflammatory cytokines
SC interferon 1A / 1B reduce relapse and lesion accumulation
→ 2nd line = plasmaphoresis / stem cell transplant
How might you symptomatically treat MS?
exercise to maintain activity & strength
neuropathic pain = amitriptyline / gabapentin
depression = SSRI
Urgen incontinence = anticholinergic medications = oxybutynin
spasticity = gabapentin / botox
What is Charcot Marie Tooth syndrome?
dysfunction in myelin or axons causes weakness and impaired sensory perception due to improper signalling
Nature of Charcot Marie Tooth syndrome? aetiology?
inherited = auto dom!
affects peripheral motor & sensory pathways
before 10 or later than 40
Pathology of CMT?
Loss of myelin on peripheral neurones OR loss of peripheral neurones
progressive loss of
→ motor in feet & legs
→ sensory in hands & feet
Present - CMT?
High foot arches = pes cavus
Distal muscle wasting = inverted champagne bottle legs
Weakness, sharp pain & numbness in hands and legs
= trip a lot, clumsy, feet slap the ground when walking, can’t run
Management for CMT?
no tx, for cause or prevent progression
physio, occup, podiatrist
ortho surgeon to correct disabling joint deformities
Differentiate Charcot Marie Tooth & MS?
MS = disease of brain & spinal cord
→ CNS
mvt, sensory, thinking
CMT = disease of peripheral nerves
→ PNS
weakness & sensory perception
signal can’t get to brain
Causes of peripheral neuropathy?
A alcohol
B B12 deficiency
C cancer & chronic kidney disease
D diabetes
& drugs - isoniazid, amiodarone, cisplatin
E every vasculitis
What are Duchenne & Becker’s muscular dystrophies
Genetic disorder characterised by progressive muscle degeneration and weakness
both → x-linked recessive
What are dystrophins?
proteins which keeps muscle cell intact
lack of dystrophins = become fragile & easily damaged
Pathophysio of Duchenne’s & Becker’s?
Duchenne = no functional dystorphins made
Becker = dystrophin protein only partially functional
Characteristic presentation of Duchenne & Becker’s muscular dystrophies?
hallmark = muscle weakness
Gower’s manoeuvre = walks hands to legs before getting up
Enlargement of calves
Difficulty jumping, running & walking, clumsy, waddling gait, lumbar lordosis (spine curve inwards)
Compare and contrast Duchenne & Becker muscular dystrophy in terms of presentation?
Duchenne = early childhood, usually 2-3, boys
→ proximal body muscle to distal
Becker = teens to early adulthood, men 5-60
→ begins hips and pelvic, thighs & shoulders
Complications of Duchenne & Becker muscular dystrophies?
Cardiomyopathy & respiratory symptoms (weakened organs)
Adrenal insufficiency (from steroids)
Growth retardation
late puberty, lack of testosterones,
Investigations for the MD’s?
Screen = Creatinine kinase
= enzyme released by muscle when damaged
= usually 10-100x value (>200)
Diagnostic = genetic testing
then test for liver function
How might you treat the muscular dystrophies?
Corticosteroids = slow progress
prednisolone
ataluren = if genetic defect
→ allows ribosome to read through premature stop codons that causes incomplete dystrophin synthesis
Supportive = bone health & hormones (from steroids), supply with vitamins
What are motor neurone diseases?
= umbrella of rare degenerative neurological illness affecting the motor neurones
→ rare progressive ultrimately fatal
Risk & pathology of motor neurone diseases?
Genetic component
→ surviving motor neurones contain abnormal protein TDP-43
Fam hx
links: smoking, heavy metal exposure, certain pesticides
How are MND classified? Examples?
Upper motor neurones, lower motor neurones, mixed neurones (ALS, progressive bulbar)
Differentiate UMN lesion from LMN lesion?
UMN = spasticity (+tone), hypereflexia, plantars,
LMN = wasting, fasciculation, absent nerve conduction
weakness corresponding to lower cord nerves
Diff = in UMN forehead will be spared = stroke
Example of an upper motor neurone disease?
Primary lateral sclerosis
= loss of Betz cells in motor cortex, mainly UMN signs, marked leg weakness & pseudobulbar palsy
Example of a lower motor neurone disease?
Progressive muscular atrophy
= weakness & wasting of distal muscle, fasciculations & absent reflexes
Example of a mixed motor neurone disease?
Amylotrophic lateral sclerosis ALS
= classic & most common
= distal & proximal muscle weakness & wasting, spasticity, hyperreflexia
Typical presentation of ALS?
Triad of
Limbs
Bulbar
Respiratory
The motor neurone disease on its own & second most common?
Progressive bulbar palsy
= only bulbar muscles = talking & swallowing
→ involves cranial nerve nuclei
Typical presentation for MNND?
Limb onset = 75%
→ distal asymmetric weakness of the arms / hands
= grip / shoulder abduction issues
- *→ lower limb symptoms**
- *= stumbling gait, foot drop,** tripping, loss of power, wasting
Typical progressive presentation of MND?
Bulbar onset (25%)
→ dysarthria, wasting & fasciculations of tongue, dysphagia, slurred speech
Respiratory (5%)
dyspnoea, orthopnoea, poor sleep, reduced appetite, weight loss
Distinguish MND from Myasthenia Gravis & Multiple sclerosis?
MND never affects eyes movements - MG
MND will not have sphincter disturbances - MS
How might you investigate motor neurone disease?
Upper = imaging, from the lesion upward
Lower = nerve conduction studies NCS / Electromyography (EMG)
ALS = + creatinine kinase
Diagnostic criteria of ALS?
El Escorial diagnostic criteria
Definite = LMN + UMN in 3 regions
Probable = LMN + UMN in 2 regions
or (LMN +) UMN in 1 region
+ EMG acute denervation in ≥ 2 limb
- *Possible** = LMN + UMN in 1 region
- *Suspected** = LMN, or UMN, only
Complications / links of MND?
Frontotemporal dementia
Death causes = respiratory failure or pneumonia
Only medication to slow progression of ALS / MND?
Riluzole
prolongs life for 3-4 months
Tx for MND muscle cramps?
1st = quinine
SE prolongs QT interval
2nd = baclofen
→ consider exercise programs
Tx for MND salivation problems?
1st = antimuscarinics
propantheline, SC glycopyrroate (less cognitive effects = preferred for cognitive impairment)
botox type A if doesn’t work
Tx for respiratory symptoms in MND?
treat reversible causes of worsening respiratory impairment before considering meds
opioids / benzodiazepines
non-invasive ventilation at home for those with respiratory impairment
Supportive measures for ALS?
Bulbar - blend food, gastrostomy
non invasive ventilation
What is corticobulbar palsy / pseudobulbar palsy?
UMN lesion of bulbar muscles due to bilateral lesions above the mid pons
Presentation of corticobulbar / pseudobulbar palsy?
Slow tongue movements & speech
jaw jerk
pharyngeal & palatal reflexes
Pseudobulbar effect
→ weeping unprovoked by sorrow
→ mood incongruent giggling
= emotional incontinence without mood change
Tx corticobulbar palsy?
dextromethorphan + quinidine
Which spinal tract is the descending upper motor neurone?
Corticospinal
decussate at the medulla
Which spinal tract is responsible for proprioception, vibration & 2 point discrimination?
Dorsal column
= ascending sensory tract
decussate at medulla
Which spinal tract is responsible for pain and temperature?
Spinothalamic tract
= ascending sensory tract
decussate IMMEDIATELT at spinal cord
What are common causes of spinal cord compression?
acute = vertebral body neoplasm
most common
Disc herniation
Disc prolapse
(bulge within the disc itself)
Presentation - spinal cord compression?
Sensory loss below the level of lesion (sensory level)
What is sciatica?
S1 nerve root compression
Sensory loss in back of leg to lateral aspect of little toe (sciatic nerve distribution)
How will L5 nerve root compression present?
Sensory loss / pain in lateral leg & medial side of big toe
Investigations for spinal cord damage?
do not delay!!
MRI = gold standard
biopsy / surgical exploration for identifying masses
Treatment for spinal cord compression?
if malignancy = IV dexamethasone
Epidural abscess = surgically decompress and antibiotics given
Neurosurg refer stat
→ decompression
laminectomy / microdisectomy
(reduce inflammation & oedema)
How many vertebrae and pairs of spinal cord are there in the spinal coloumn?
33 vertebrae, 31 spinal cords
7 (8) cervical, 12 thoracic, 5 Lumbar, 5 sacral, 4 (1) coccygeal
How many intervertebrae discs are there?
23
Where does the spinal cord end?
L2, conus medullaris
What is the cauda equina?
5 lumbar 5 sacral 1 coccygeal
nerve roots distal to the level of termination at L1/L2
LMN!!!
Muscular presentation of someone affected by cauda equina?
Flaccid & areflexic
Causes of cauda equina?
Spondylolisthesis = top vertebra slips forward (sink into body), nerve root comes above the vertebra below
Herniation of lumbar disc
L4/5 or L5/S1
Tumours / mets
spinal stenosis / ankylosing spondylitis
trauma / post op haematoma
Present cauda equina?
Variable leg weakness
→ flaccid & areflexic (LMN signs)
Bilateral sciatica
Saddle anaesthesia
Bladder / bowel dysfunction, erectile dysfunction
Investigations of cauda equina?
MRI to localise lesion
knee flexion - tests L5-S1,
ankle plantar flexion tests S1-S2
straight leg raising = L5 S1
femoral stretch = L4
Treatment for cauda equina syndrome?
= EMERGENCY
refer to neuro immediately
decompression of the nerve stat to avoid irreversible paralysis
→ microdisectomy, epidural steroid for pain, surgical spine fixation if slipped disk, spinal fusion = reduce pain from motion → nerve root
