Neuro Flashcards
Bell’s palsy (facial nerve paralysis)
Prognosis
most people with Bell’s palsy make a full recovery within 3-4 months
if untreated around 15% of patients have permanent moderate to severe weakness
Ix:
lower motor neuron facial nerve palsy → forehead affected
Also,
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis
Mx = oral prednisolone within 72 hours of onset
Eye care = lube, tape and artificial tears
For a patient with a Bell’s palsy, if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT!
Query add antivirals?
Cluster headache (intense sharp, stabbing pain around one eye, occurs once or twice a day, each episode lasting 15 mins - 2 hours, for 4-12 weeks accompanied by redness, lacrimation, lid swelling nasal stuffiness
miosis and ptosis in a minority)
RF’s?
Ix = MRI with gadolinium contrast
RF’s = young male smoker with positive family history
Mx = refer to neurologist
Acute = triptan + O2
prophylaxis = verapamil
Encephalitis (caused by HSV-1!
meningitis vs enceph? - enceph has psychiatric sx or altered mental status - e.g. focal/absence seizure)
Ix:
CSF
lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses
MRI = medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
normal in one-third of patients
EEG = lateralised periodic discharges at 2 Hz
Mx = IV aciclovir should be started in all cases of suspected encephalitis
Epilepsy (t/c, focal, absence, myoclonic, a/tonic)
Focal can present with aura
simple = aware, complex = no memory of the seizure + automatisms
After this focal(aura) seizure this can then develop into a full generalised seizure!
Generalised tonic-clonic seizures
m = sodium valproate*
f = lamotrigine or levetiracetam
girls < 10yo or women who are unable to have children = sodium valproate
Focal seizures (previously called partial)
1st = lamotrigine or levetiracetam
2nd = carbamazepine, oxcarbazepine or zonisamide
Absence seizures (Petit mal)
1st = ethosuximide
2nd = same as gen-ton-clon
m = sodium valproate
f = lamotrigine or levetiracetam
carbamazepine may exacerbate absence seizures
Myoclonic seizures
m = sodium valproate
f = levetiracetam
Tonic or atonic seizures
m = sodium valproate
f = lamotrigine
men take sodium valproate for everything apart from focal
Women take leve/lamo for everything apart from (myo = leve, a/tonic = lamo)
“myo-lev!, miya-ha-ha” drinking a tonic in a lambo
Focal and absence are the only special ones
*Caution should be exercised when combining sodium valproate and lamotrigine as serious skin rashes such as Steven-Johnson’s syndrome may be provoked
Extradural haemorrhage
Ix = CT head
Mx = ?
Guillain-Barré syndrome
Caused by an immune attack on the
nerve cells of the peripheral nervous system and their support structures
Ix = Multifocal decreased motor conduction speed with/without conduction block
Miller Fisher syndrome = variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia.
The eye muscles are typically affected first
usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
anti-GQ1b antibodies are present in 90% of cases
Mx: 1st = IV Ig 2nd = plasmapharesis
Horner’s Syndrome
Ix = miosis (small pupil), ptosis, anhidrosis (loss of sweating one side)
enophthalmos* (sunken eye)
apraclonidine drops (an alpha-adrenergic agonist) can be used.
causes pupillary dilation in Horner’s syndrome due to denervation supersensitivity but produces mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft
Huntington’s disease
Ix:
Genetics
autosomal dominant - trinucleotide repeat disorder: repeat expansion of CAG (n huntingtin gene on chromosome 4) - results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia leading to hyperkinetic movements.
Anticipation - as Huntington’s disease is a trinucleotide repeat disorder, the disease presents at an earlier age in successive generations
Features typical develop after 35 years of age
- chorea
- personality changes (e.g. irritability, apathy, depression) and intellectual impairment
- dystonia
- saccadic eye movements
Hydrocephalus
Normal pressure hydrocephalus is a unique form of non-obstructive hydrocephalus characterised by large ventricles but normal intracranial pressure. The classic triad of symptoms is wet wacky and wobbly (incontinence, dementia, and disturbed gait)
Ix:
1st line = CT head
MRI may be used to investigate hydrocephalus in more detail, particularly if there is a suspected underlying lesion
Lumbar puncture* is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure
*Lumbar puncture must not be used in obstructive hydrocephalus! Since the difference of cranial and spinal pressures induced by the drainage of CSF will cause brain herniation.
Mx = external ventricular drain (EVD) into the right lateral ventricle and drains into a bag at the bedside
A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum
Obstructive hydrocephalus = surgery on the obstruction
Idiopathic intracranial hypertension - fat, female, on COMAAR;
Ciclosporin
Ocp,
Mineralocorticoids,
Amiodarone,
Antibiotics (tetracyclines)
Retinoids,
Ix = (headache + papilloedema) blurred vision, enlarged blind spot, sixth nerve palsy may be present
Mx = weight loss
diuretics e.g. acetazolamide (carbonic anhydrase inhibitor)
topiramate is also used (causes weight loss)
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
Meningitis (Fever, neck pain, confusion (bacterial=hours, viral=days)
meningitis becomes meningococcal septicaemia when the pathogen spreads into the blood and causes systemic sx
Sensorineural hearing loss is the most common complication following meningitis
Ix = Lumbar puncture
LP is delayed if;
Signs of sepsis/rash
Resp/cardiac compromise
Bleeding risk
Raised ICP
focal neurological signs
papilloedema
Seizures
GCS ≤ 12
Mx: ab’s given as a priority if LP isn’t possible, to treat potential septicaemia!
<50yo = IV cefotaxime* + IV dexameth
>50yo = cefotaxime+amox+dexameth
Contacts of patients with meningococcal meningitis = Oral ciprofloxacin or rifampicin
over 50s men(ingitees) are CADs
- benpen in the community!
Migraine (Unilateral, severe headache, phonophobia 4-72hrs)
Ix:
UMN = (URTI) increased tone+reflexes, decreased power
LMN = everythings lower (tone, reflexes, power)
MRI, LP, FBC,
Mx:
Acute = oral triptan, NSAID/paracetemol
prophylaxis(>2attacks/month) = topiramate/propranolol
Motor neurone disease (ie. ALS and bulbar palsies - mixed UMN+LMN sx but no sensory deficit)
Brisk reflexes in a wasted limb is classic for MND
Ix:
MRI, EMG (fasiculations), LP
Mx = Riluzole
Amytriptyline (drooling)
baclofen/botulin (spasticity)
NG/PEG (dysphagia)
Analgesia (pain)
ventilate (resp)
AL’s wearing a R.A.B coat - Riluzole, amytriptyline, baclofen
UMN can be tested by hoffmans reflex - flicking the middle finger and if the thumb twitches, its an UMN lesion
or Babinskis - upgoing plantar reflex = UMN
Multiple sclerosis (AI attack causing demyelination in the cns, leading to relapsing and remitting)
UMN/LMN?
Also, which cells are affected?
Factors influencing severity of disease?
Ix = Lesions disseminated in time and space. MS TEAMS - Tingling, Eye*, Ataxia, Motor
May involve UMN, senosry loss and cerebellar ataxia but NEVER involves LMN
MRI =
high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum
LP
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG
Visual evoked potentials
delayed, but well preserved waveform
Mx:
Acute = methylpred (predators on MS TEAMS)
Chronic = DMARD’s (IFN-B, glatiramer) + natali/alemtu-zumab
Cells affected = Oligodendrocytes
Factors predicting a less severe disease;
1.Female,
2. <25 yo,
3. Optic neuritis/ sensory, rather than
cerebellar symptoms on initial presentation,
4. A long interval (>1 year)
between relapses
5. Few lesions on MRI
*Often presents with opthalmoplegia - diplopia when asked to look right,
the left eye stays in the midline but the right eye moves right and starts jerking
Myasthenia gravis
Interestingly, MG is hypersensitive to rocuranium (as it antaganises post-synaptic nicotinic receptors which are already reduced in MG)
and is resistant to suxamethonium (which works by over-depolarising nicotinic receptors, of which there are few in MG)
Ix = single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal
anti-Ach-r ab’s
anti-muscle-specific tyrosine kinase ab’s
Mx:
1st = pyridostigmine (long-acting acetylcholinesterase inhibitors)
immunosuppression (pred) is usually not started at diagnosis, but the majority of patients eventually require it in addition to long-acting acetylcholinesterase inhibitors:
azathioprine, cyclosporine, mycophenolate mofetil may also be used
Thymectomy
Management of myasthenic crisis = plasmapheresis + IV IG’s
Maya working at the pyramids surrounded by (pred)ators
Neurofibromatosis
Ix: NF2 has vestibular schwannomas
Parkinson’s disease
Parkinson’s disease should only be diagnosed and managed by a specialist. Therefore, the GP must make a neurology referral.
Ix:
MRI (to rule out vascular causes)
DAT-scan - to trace DA
Mx:
1st = Levodopa, MAO-Bi (selegiline), DA agonists (ropinirole)
2nd = COMTi (entacapone)
Raised intracranial pressure
Ix:
neuroimaging (CT/MRI)
Invasive ICP monitoring
Catheter in lateral ventricles to monitor the pressure is used to (collect+drain CSF)
A cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP
Mx:
Investigate and treat the underlying cause
head elevation to 30º
IV mannitol may be used as an osmotic diuretic
controlled hyperventilation - aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain
CSF removal (catheter, LP’s, ventriculoperitoneal shunt (for hydrocephalus))
Spinal cord compression (incl. cauda equina)
Ix = MRI spine within 24 hours of presentation
Mx = high-dose oral dexamethasone
Urgent oncological assessment for consideration of radiotherapy or surgery
If there are multiple lesions and pt is too frail for surgery. Radiotherapy is
the best treatment option!
Spine: Radiculopathy
Stroke (ischaemic and haemorrhagic)
Low GCS or HIGH BP precludes thrombolytic treatment
Ix = A non-contrast CT head scan - Iooking for is it ischaemic/haemorrhagic?
Acute ischaemic strokes = areas of low density in the grey and white matter of the territory. These changes may take time to develop
other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately
Acute haemorrhagic strokes = areas of hyperdense material (blood) surrounded by low density (oedema)
Mx:
Acute = 300mg aspirin
<4.5hrs = alteplase
<4.5hrs + PCA = alteplase + thrombectomy
<6hrs thrombectomy
Secondary prevention:
No AF = Clop (if clop is CI, then aspirin+dipyridamole, if aspirin is CI then just dipyridamole)
AF = apixaban/warf
If they’re eating put them NBM immediately
Subarachnoid haemorrhage
Ix:
1st - non-contrast CT
Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
if CT head is done within 6 hours of symptom onset and is normal
new guidelines suggest NOT doing a lumbar puncture and consider an alternative diagnosis
if CT head >6hrs after symptom onset and is normal -> do an LP
Timing wise the LP should be performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown)
Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure
If the CT shows evidence of a SAH = Referral to surgery as soon as SAH is confirmed
After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)
Mx = supportive + Nimodipine (prevents vasospasm/aneurysm)
bed rest + analgesia
Venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)
Aneurysm treated using coil/clipping by a neurosurgeon
Subdural haemorrhage
Tension headache (bilateral tight band)
Ix:
Not associated with aura, nausea/vomiting or aggravated by routine physical activity
may be related to stress
may co-exist with migraine
Chronic tension-type headache = 15+ days per month
Mx 1st = aspirin, paracetamol/NSAID
Prophylaxis: = ‘up to 10 sessions of acupuncture over 5-8 weeks’
Transient ischaemic attacks (TIA)
Ix = MRI on the same day as the assessment
Carotid doppler = to view atherosclerosis emboli to see if they’re a candidate for carotid endarterectomy!
Mx:
acute = 300mg aspirin
prevention: 1st= Clop
2nd = Dipyridamole
3rd = Aspirin (75mg)
lipid modification = atorvastatin 20–80 mg daily - the aim of statin therapy is to reduce non-HDL cholesterol by more than 40%
Carotid stenosis > 70% = endartectomy
Trigeminal neuralgia (a unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve)
The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously
small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
the pains usually remit for variable periods
Red flag symptoms and signs suggesting a serious underlying cause:
Sensory changes
Deafness or other ear problems
History of skin/oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years
Mx = Carbamazepine
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
Wernicke’s encephalopathy
Ix = decreased red cell transketolase + MRI
Mx = thiamine
Rinne and Webers Test
Weber = middle of the head
Rinne = mastoid process
1st = Weber
Localises to louder side
2nd = Rinne
Air>Bone = normal
Bone>air = conductive loss
Rinne and Webers Test
Weber = middle of the head
Rinne = mastoid process
1st = Weber
Localises to louder side
2nd = Rinne
Air>Bone = normal
Bone>air = conductive loss
Alzheimers (make card)
Which part of the brain is most affected in early alzheimers?
temporal lobe!
Vestibular neuronitis = a cause of vertigo that often develops following a viral infection.
Features
recurrent vertigo attacks lasting hours or days
nausea and vomiting may be present
horizontal nystagmus is usually present
NO hearing loss or tinnitus
Differential diagnosis
viral labyrinthitis
posterior circulation stroke: the HiNTs exam can be used to distinguish vestibular neuronitis from posterior circulation stroke
Mx:
Severe = buccal or IM prochlorperazine
Less severe = a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine)
Chronic = vestibular rehabilitation exercises
BPPV (Benign paroxysmal positional vertigo)
(BPPV) is one of the most common causes of vertigo encountered. It is characterised by the sudden onset of dizziness and vertigo triggered by changes in head position. The average age of onset is 55 years and it is less common in younger patients.
Features
vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre, indicated by:
patient experiences vertigo
rotatory nystagmus
BPPV has a good prognosis and usually resolves spontaneously after a few weeks to months. Symptomatic relief may be gained by:
Epley manoeuvre (successful in around 80% of cases)
teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises
Reversal of Neuro-muscular blocking drugs used in muscle paralysis for mechanical ventilation in surgery? (Non-depolarising)
Neostigmine!
What signs indicate a lesion in the;
Basal ganglia
Cerebellum
Internal capsule
Motor cortex
Pyramidal tracts
?
Basal ganglia – to initiate and stop movement
Cerebellum – fine movement, gait, proprioception
Internal capsule – will give purely motor or purely sensory
Motor cortex -
Pyramidal tracts – tracts of the spine?
What is Brown Sequard syndrome?
Hemisection of the cord is also known as Brown–Séquard syndome.
This results in ipsilateral paralysis and loss of light touch and vibration
sensation and contralateral loss in pain and temperature below the point
of the lesion.
The spinothalamic tracts cross at the level of the cord, so
sensation to pain and temperature is lost in the contralateral limbs
Whats the differentiator for orthostatic vs vasovagal syncope?
Orthostatic = reduced cerebral
perfusion as the patient moves from lying to standing. Symptoms are
similar to vasovagal in that the patient may become pale and describe ‘the
lights or sound dimming’. Perfusion is restored after the patient collapses
and unconsciousness lasts no more than seconds or a couple of minutes
with full recovery.
However, vasovagal epsiodes can be brought on by
sleep or food deprivation, hot or emotional environments, Valsalva
manoeuvre (such as straining) and are not as closely related to position!
What are the 9 contraindications for thrombolysis?
contraindications for thrombolysis are:
- onset of symptoms more than 3
hours ago, - seizures at presentation,
- uncontrolled blood pressure (over
180/110), - previous intracranial bleed,
- lumbar puncture in the last week,
- ischaemic stroke or head injury in the last three months,
- active bleeding (not menstruation),
- surgery/major trauma (including CPR) within the last 2 weeks
- non-compressible arterial puncture within the last week.
Status epilepticus
What is it?
Mx?
Status epilepticus is defined as:
a single seizure lasting >5 minutes, or
>= 2 seizures within a 5-minute period without the person returning to normal between them
This is a medical emergency. The priority is the termination of seizure activity, which if prolonged will lead to irreversible brain damage.
Management
ABC
airway adjunct
oxygen
check blood glucose
1st = IV benzodiazepines such as diazepam or lorazepam
2nd = phenytoin or phenobarbital infusion
3rd = general anaesthesia
in the prehospital setting PR diazepam or buccal midazolam may be given
in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes
If ongoing (or ‘established’) status it is appropriate to start a second-line agent
If no response to phenytoin (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.
4 Causes of combined UMN+LMN symptoms?
B12 deficiency
Cord compression (chord+roots) spondylitis/syringomyelia
Motor neurone disease
Freidreich’s ataxia - both cord and peripheral nerve involvement accompany cerebellar degeneration. These patients also have sensory loss, pes cavus and may have complications such as diabetes and hypertrophic cardiomyopathy
3 scenarios for the 3 intracranial haemmorrhage types
- Convex (lenticular) haematomas are seen in extradural haemorrhages
as the blood is trapped between the dura and the skull. These most
commonly occur as a result of trauma and rupture of the middle meningeal
artery. - Crescent-shaped haematomas indicate the blood is between the dura and arachnoid. Subdural haemorrhages occur as a result of bleeding from bridging veins, more commonly seen in the elderly and alcoholics as the veins are stretched from cerebral atrophy.
- Blood along the sulci and fissure indicates that it is located between the arachnoid and the pia. Subarachnoid haemorrhages present clinically as a thunderclap headache which may be associated with reduced GCS and seizures
Herpes Simplex encephelitis px?
AI enceph hx?
CT head showing temporal lobe changes (hypodensities) - think herpes simplex encephalitis
Autoimmune encephalitis is typically the result of a paraneoplastic syndrome (usually secondary to small cell lung cancer or ovarian teratoma).
Phenytoin SE’s?
Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures
Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia
Idiosyncratic
fever
rashes, including severe reactions such as toxic epidermal necrolysis
hepatitis
aplastic anaemia
drug-induced lupus
Lesions and their signs on examination
Cerebellar hemisphere - finger-nose ataxia
Basal ganglia - Hypokinetic (e.g. Parkinsonism) or hyperkinetic (e.g. Huntington’s)
Parietal lobe - sensory symptoms, dyslexia, dysgraphia
Frontal lobe - motor symptoms, expressive aphasia, disinhibition
Cerebellar vermis lesions = Gait ataxia
Lateral medullary syndrome cause and px?
Basilar artery?
Webers syndrome?
The Posterior Inferior Cerebellar Artery (PICA) supplies the lateral medulla and occlusion of the left vessel will cause;
- Left-sided Horner’s syndrome,
- ataxia,
- facial numbness with contralateral body numbness
Basilar artery = locked in syndrome
Webers = Branches if the PCA supplying the midbrain, occlusion causes;
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Lambert-Eaton sx + mx?
Caused by an antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.
Also which cancer is it associated with?
Opposite to MG - repeated muscle contractions lead to increased muscle strength
Autonomic symptoms(dry mouth, impotence, difficulty micturating),
Limb-girdle weakness (manifesting as a waddling gait),
Hyporeflexia
cancer = Small cell lung cancer
mx = pred/aza immunosuppression
Difference between posterior and pontine stroke?
Pontine haemorrhage commonly presents with reduced GCS, paralysis and bilateral pin point pupils
Posterior = (ipsilateral?) cranial nerve palsy and contralateral motor and/or sensory deficits, nystagmus, cerebellar dysfunction, vertigo, or isolated homonymous hemianopia
Difference between Wernickes and Korsakoffs?
Wernickes = classic triad of;
- ophthalmoplegia/nystagmus, 2. ataxia
- encephalopathy
Korsakoffs = amnesia + confabulation without any neurological signs!
What clinical sign could be examined to further evaluate whether a lower leg weakness is an organic or functional presentation?
To rule in/out conversion disorder
Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction.
If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis.
If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.
5 types of a/dysphasia?
wernickes
Brocas
Global
Anomic
Conduction
Broca’s aphasia results in non-fluent, laboured and halting speech.
Wernicke’s aphasia results in neologisms and nonsense sentences which is fluent.
Global aphasia causes severe expressive and receptive deficits.
Anomic aphasia is a deficit of expressive language which results primarily in word finding difficulties
Conduction dysphasia: speech fluent, but repetition poor. Comprehension is relatively intact
When there is a mix of UMN and LMN signs in a patient, always consider Subacute degeneration of the chord. What is SCDC?
Subacute combined degeneration of the cord involves degeneration of the posterior and lateral columns of the spinal cord, often due to vitamin B12 deficiency.
Damage to the posterior columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).
Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).
Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).
Cerebral abscess
Ix = CT scan
Mx:
surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
IV antibiotics: IV 3rd-generation cephalosporin(cefotaxime) + metronidazole
strep = cefuroxime + metro
staph = cefuroxime + floclox
intracranial pressure management: e.g. dexamethasone
Syringomyelia
In Syringomyelia a fluid filled cyst forms in spinal cord and expands over time. This causes slowly progressive neurological symptoms. Syringomyelia is also associated with the Arnold-Chiari malformation (congenital issue where the lower part of the brain pushes down on the spinal chord)
Syringomyelia starts with the lack of pain sensation in the arms before giving
more prominent lower motor neuron weakness in the arms, and then later upper motor neuron weakness in the legs
Features
a ‘cape-like’ (neck, shoulders and arms)
loss of sensation to temperature but the preservation of light touch, proprioception and vibration
classic examples are of patients who accidentally burn their hands without realising
this is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected
spastic weakness (predominantly of the lower limbs)
neuropathic pain
upgoing plantars
autonomic features:
Horner’s syndrome due to compression of the sympathetic chain, but this is rare
bowel and bladder dysfunction
scoliosis will occur over a matter of years if the syrinx is not treated
Ix = full spine MRI with contrast to exclude a tumour or tethered cord
a brain MRI is also needed to exclude a Chiari malformation
Treatment will be directed at treating the cause of the syrinx.
In patients with a persistent or symptomatic syrinx, a shunt into the syrinx can be placed.
How to tell the difference between bacterial and viral meningitis
Everything is more mild in viral meningitis!
Onset and Progression of Symptoms:
Bacterial Meningitis: Symptoms typically develop rapidly and progress quickly, often within hours. The condition can be severe and life-threatening.
Viral Meningitis: Symptoms generally have a more gradual onset, evolving over a period of days. The progression is usually less severe compared to bacterial meningitis.
Fever:
Bacterial Meningitis: High fever is commonly present, often exceeding 38.5°C (101.3°F).
Viral Meningitis: Fever is generally lower grade, often below 38.5°C (101.3°F).
Presence of Neck Stiffness:
Bacterial Meningitis: Neck stiffness (nuchal rigidity) is frequently observed and may be severe.
Viral Meningitis: Neck stiffness can be present but is typically milder compared to bacterial meningitis.
Severity of Headache and Other Symptoms:
Bacterial Meningitis: Headache is usually severe and persistent. Other symptoms may include nausea, vomiting, photophobia (sensitivity to light), and altered mental status.
Viral Meningitis: Headache is generally milder compared to bacterial meningitis. Other symptoms may include mild nausea, vomiting, and sensitivity to light.
CSF Analysis:
Bacterial Meningitis: Cerebrospinal fluid (CSF) analysis typically reveals elevated white blood cell count (predominantly neutrophils), increased protein levels, and low glucose levels.
Viral Meningitis: CSF analysis typically shows increased lymphocytes (lymphocytic pleocytosis), normal or slightly elevated protein levels, and normal glucose levels.
Other Clinical Signs and Symptoms:
Bacterial Meningitis: Patients may present with more severe signs, such as seizures, focal neurological deficits, altered consciousness, and petechial or purpuric rash.
Viral Meningitis: These severe signs are less common, and a rash, if present, is usually maculopapular and non-purpuric.
