Neurology Flashcards
What are some of the key side effects of phenytoin?
Peripheral neuropathy - numbness and reduced sensation in glove and stocking distribution
PDGF increased expression causing:
Gingival hyperplasia - bleeding gums
Hirsutism and coarse facial features
Altered folate metabolism - megaloblastic anaemia
Lymphadenopathy
MOA of phenytoin
Acute SE’s
Binds to Na channels increasing their refractory period
Acute - dizziness, diplopia, nystagmus , slurred speech, ataxia
Later acute - confusion and seizures
Define Bell’s Palsy
What is the cause of Bell’s palsy
Describe the key features
Bells Palsy - acute, unilateral idiopathic facial nerve paralysis. It is a diagnosis of exclusion made in those with facial paralysis which fully evolves in 72 hours.
Aetiology - unknown but probable viral aetiology.
Key features:
Single episode of unilateral facial paralysis
With abscence of constitutional symptoms ( fever/ rash/ headache/ arthralgia think alternative diagnosis e/g/ Lymes disease).
Facial nerve palsy involving all nerve branches ( if unequal distribution of facial weakness rules out bells palsy) ( no forehead sparing as in UMN lesion).
Dry eye ( loss of parasympathetic innervation of tear duct and loss of blink function) ( can progress to corneal ulceration)
post auricular pain / otalgia ( severe pain suggests herpes zoster of facial nerve)
Hyperacusis
altered taste
Most common 15- 45 yrs and pregnant women
What nerve is affected in foot drop?
Where is this nerve derived from?
Where is it commonly injured?
What are the other features of nerve damage to this nerve?
Common peroneal nerve
Common peroneal nerve is derived from the sciatic nerve which splits into the tibial and common peroneal nerve.
Injury most commonly occurs at the neck of the fibula.
( Anatomy - common fibular nerve splits into the superficial fibular nerve and the deep fibular nerve. Superficial fibular nerve innervates the muscles of the lateral compartment of the leg Fibularis longus and brevis, acts to evert the foot. Deep fibular nerve innervates muscles of the anterior compartment of the leg, tibialis anterior, extensor digitorum longus and extensor hallucis longus.)
Features of common peroneal nerve injury:
- weakness of dorsiflexion, eversion and extensor hallucis longus
- sensory loss over the dorsum of the foot and lower lateral part of the leg
wasting of anterior tibial and peroneal muscles
Management of Bells Palsy
All patients should receive oral prednisilone within 72 hours of the onset of Bell’s palsy.
Clinical debate on the addition of antivirals. Alone is not recommended but in combination with steroid may be of benefit. In severe facial palsy may be of benefit.
Eye care - important to prevent exposure keratopathy. Prescription of artificial tears and eye lubricants. If patients are unable to close the eye at bedtime they should tape it closed with microporous tape.
Follow up - if paralysis shows no improvement in 3 weeks then refer urgently to ENT.
Prognosis - most people make a full recovery within 3-4 months. Untreated 15% of patients have a permanent moderate to severe weakness.
Key management points in Stroke
1) BM, hydration, oxygen sats and temperature should be maintained within normal limits
2) BP should not be lowered in acute phase unless there are complications
3) Aspirin 300 mg orally or rectally given as soon as possible if haemorrhagic stroke has been excluded
4) AF in stroke - anticoagulants should not be started until brain imaging has excluded haemorrhage and not for 14 days since onset of ischaemic stroke
5) if cholesterol > 3.5 mmol/ L patients should be started on a statin. Delay for 48 hours due to risk of haemorrhagic transformation.
When is thrombolysis indicated in stroke?
Thrombolysis indicated if - within 4.5 hrs of the onset of stroke symptoms AND haemorrhage has been definitively excluded.
What are the absolute contraindications to thromboylsis?
Absolute:
Seizure at onset of stroke
Previous intracranial haemorrhage
Intracranial neoplasm
suspected SAH
Stroke/ TBI in past 3 months
LP in past 7 days
GI bleed in last 3 weeks
Active bleeding
Pregnancy
Oesophageal varices
uncontrolled HTN > 200 mmHg
what are the relative contraindications to thrombolysis?
Concurrent anticoagulation INR > 1.7
Known coagulopathy
Active haemorrhagic diabetic retinopathy
suspected intracardiac thrombus
major surgery in past 2 weeks
Indications for Thrombectomy in acute stroke?
1) clinical status - must have a good pre functional status prior to the stroke ( NIHSS > 5) ( less than 3 on modified rankin scale).
2) Within 6 hours of symptom onset ( plus intravenous thromboylsis if within 4.5 hours)
3) Type of stroke: Ischaemic and
–> Proximal anterior circulation stroke proven on CT angiography or MR angiography
OR 4) Within 6-24 hours of symptom onset for:
–> Proximal anterior circulation stroke on CTA/MRA PLUS potential to salvage brain tissue as shown by CT perfusion or diffusion weighted MRI.
–> CONSIDER in patients with proximal posterior circulation strokes ( basilar or posterior cerebral artery) on CTA/MRA AND potential to salvage brain tissue on diffusion weighted MRI or CT perfusion.
Aspirin in stroke:
Offer antiplatelet as soon as possible but within 24 hours to any patient with acute stroke that has had haemorrhage excluded by imaging. In those undergoing
thrombolysis Aspirin is usally delayed for 24 hours.
Aspirin daily for 2 weeks after stroke - 300 mg orally/rectally and then start definitive lon term antithrombotic therapy after 2 weeks OR Aspirin 300 mg as loading dose, then 75 mg OD for 21 days AND clopidogrel 300 mg orally as loading dose then 75mg OD for 21days. After three weeks DAPT then monotherapy with clopidogrel lifelong. Aspirin if unable to tolerate clopidogrel. ( In patients without AF).
( Dont forget PPI cover when on DAPT/ aspirin if previous intolerance)
Other secondary prevention strategies in acute stroke patients
1) Antiplatelet therapy - DAPT for three weeks then lifelong single APT.
2) High dose statin
3) AntiHTN - ACEi/ thiazide or long acting Ca channel blocker
4) Anticoagulation - in patients with non valvular AF offer DOAC 1st line. In those with valvular AF/ mechanical heart valves then warfarin with target INR 2.5 ( range 2-3) .
General management of acute stroke - thombolysis NOT contraindicated
1) Thombolysis NOT contraindicated
1a) Then IV alteplase within 4.5 hours of onset and intracranial haemorrhage excluded. Must monitor blood sugar, exclude hypoglycaemia ( stroke mimic) and hyperglycaemia - associated with bleeding. (Tenecteplase is a second option, on specialist advice).
1b) Consider Mechanical thrombectomy - within 6 hours of symptom onset if patient had previous good functional status and proven occlusion of proximal anterior circulation causing neurological deficit/ confirmed proximal large intracranial artery occlusion and potential to salvage brain tissue on perfusion imaging.
1c) antiplatelet agent - 24 hours after thrombolysis - DAPT for 3 weeks then single agent.
1d) VTE prophylaxis with IPC
1e) high intensity statin ( after 48 hour) atorvastatin 20-80 mg OD
General management of acute stroke - thrombolysis IS contraindicated
1a ) Consider mechanical thrombectomy alone in patients whom thrombolysis is contraindicated but presenting within 6 hrs of symptom onset, confirmed occlusion of proximal anterior circulation / proximal posterior circulation ( and potential to salvage brain tissue as shown by perfusion imaging) and no previous disability.
1b) Antiplatelet agent - 300 mg Aspirin once haemorrhagic stroke ruled out. Add second antiplatelet agent ( clopidogrel) for 3 weeks then continue clopidogrel lifelong. ( Unless AF then 2 weeks then consider anticoagulation).
1c) VTE prophylaxis IPC and early mobilisation
1d) High intensity statin - Atorvastatin 20-80 mg
When do neurosurgeons need to be involved in acute stroke?
Referal for any patients with large middle cerebral artery territory infarct or large infarctions affecting the cerebellum.
Those with middle cerebral artery infarct may need decompressive hemicraniectomy
Those wtih large cerebellum infarctions may need placement of an EVD or posterior fossa craniectomy.
This patient group are at risk of developing oedema and elevated ICP. Oedema compromises blood flow and increases risk of herniation
Supportive care in acute stroke
Monitor GCS - any evidence of reduced GCS/ seizures suspect haemorrhagic stroke.
Blood glucose - maintain 4-11 mmol.
Blood pressure - antihypertensives given only if there is a hypertensive emergency ( encephalopathy, nephropathy, cardiac failure, aortic dissection, preeclampsia or eclampsia). Otherwise in patients not treated with thromolysis/ thrombectomy and BP > 220 then CAREFUL bp reduction of 15% in 24 hours.
Oxygen - maintain sats
Hydration - may need support
Cardiac - ECG or 24 hour monitor ( exclude AF)
ICP monitoring - any evidence of reduced GCS/ severe headache/ vomiting or sudden increase in BP –> urgent repeat CT head
Seizures - levetiracetam / sodium valproate
Temperature - maintain normal, paracetamol for pyrexia
What is Wernicke’s encephalopathy?
What are the causes?
What are the features?
What are patients at risk of developing?
Wernicke’s encephalopathy is a neuropyschiatric disorder caused by thiamine deficiency. Most commonly seen in alcoholics.
Causes - EtOH excess, persistent vomiting, stomach CA, dietary deficiency.
Features: Classic triad of CAN ( confusion, ataxia and nystagmus. )
Encephalopathy - confusion, indifference and inattention
Ataxic gait
Nystagmus and opthalmoplegia often lateral rectus palsy and conjugate gaze palsy.
Peripheral sensory neuropathy
Diagnosis - clinical, MRI plus red cell transketolase ( RC transketolase measures amount of B1 available to RBCs).
Patients are at risk of developing Wernicke- Korsakoff syndrome which is characterised by the addition of antero and retrograde amenesia plus confabulation
What is degenerative cervical myelopathy?
Degenerative cervical myelopathy (DCM), a specific syndrome of neurological deficit in the upper and lower extremities resulting from spinal cord pressure in the cervical spine, due to degenerative changes in disc and/or facet joints.
Degenerative cervical myelopathy is a loss of neurological function from pressure on the spinal cord in the cervical region. Often secondary to OA of the cervical spine. Loss of function can be painful but there is usually a painless reduction in UL function, often noticed as increased clumsiness or loss of fine motor function.
How does Degenerative cervical myelopathy present?
Presentation can be variable:
- Pain in the cervical region (spontaneous onset in cervical sponydlosis)
-Pain in UL/ LL
-Loss of motor function - loss of digital dexterity, arm or leg weakness leading to impaired gait and imbalance
-Loss of sensory function - numbness
-loss of autonomic function - urinary and faecal incontinence and or impotence
- Hoffman’s sign - reflex test for cervical myelopathy, flicking the distal IP in one finger, positive test in reflex flexion of the other fingers in that hand.
OE:
Increased reflexes (UMN sign of cervical myelopathy)
Distal hand weakness
Gait ataxia
Gold standard ix for degenerative cervical myelopathy?
Management
MRI of cervical spine
mx- urgent referral to specialist spinal services - neurosurgery or orthopaedic spinal surgery.decompressive surgery is the only effective treatment. It has been shown to prevent disease progression. Close observation is an option for mild stable disease, but anything progressive or more severe requires surgery to prevent further deterioration. Physiotherapy should only be initiated by specialist services, as manipulation can cause more spinal cord damage.
SE of sodium valproate
Teratogenic - NT defects, ND delay
P450 Inhibitor
N, increased appetite, weight gain
alopecia
ataxia
tremor
hepatotoxic
pancreatitis
thrombocytopenia
hyponatraemia
What is MND?
What subtypes are there?
MND - progressive ultimately fatal condition where there is progressive loss of motor neurones in the cortex, brainstem and ventral spinal cord.
ALS ( Amyotrophic lateral sclerosis) is the most common form and presents with a combination of both upper and lower motor neurone signs. It usually involves one segment of the neuroaxis before spreading.
Others:
Progressive bulbar palsy - second most common form, loss of muscles involved in talking and swallowing.
Progressive muscular atrophy ( mostly LMN loss )
primary lateral sclerosis - loss of voluntary motor
Typical features of MND
Usually > 40 yrs
Family hx
Progressive degeneration of both upper and lower Motor neurones - sensory is spared.
Progressive muscle weakness, often noticed UL first. Usually asymmetrical.
Fatigue when exercising
Fasiculations
muscle wasting
Clumsiness / dropping objects / increased falls
Slurred speech
Swallowing difficulties
Painful muscle spasms
unsteady gait, difficulties with posture, head drop, difficulty arising from seating/ climbing stairs
Signs of MND
Signs of both lower and upper motor neurone loss:
Lower:
Atrophy
Fasciculations
Reduced tone
Reduced reflexes
Upper:
Spasticity/ increased tone
Brisk reflexes
Upgoing plantar responses
Driving rules in TIA / stroke?
Stroke or TIA - 1 month off driving. May not need to inform DVLA if no residual neurological deficit.
Multiple TIA over short period - 3 months off driving & inform DVLA
DVLA rules for neurosurgery conditions
1) craniotomy for meningioma - 1 year off driving, if benign and never presented with seizures then may consider at 6 months.
2) pituitary tumour - 6 months for craniotomy, for transphenoidal - as long as no residual impairment
DVLA rules in epilepsy
1st seizure - 6 months off if no anatomical abnormality on imaging an no definite epileptiform activity on EEG. If these conditions are not met then increased to 12 months
Established epilepsy - may qualify if seizure free for 12 months. If no seizures for 5 years then til 70 licence can be applied for.
Withdrawal of antiepileptics - should not drive for 6 months after last dose and whilst medication is being withdrawn
Clinical features of Cluster headaches
Unilateral headache lasting 15 mins - 180 mins, intense and stabbing
associated with hyperactivity of parasympathetics and low sympathetic activity.
Pain typically around orbit / temporal areas
Can occur up to 8 /day
PNS activation - lacrimation, conjunctival injection ( inflammation of the blood vessels in the conjunctiva), rhinorrhoea, eyelid and facial swelling, aural fullness ( fullness in ear), facial sweating, redness
Partial horner syndrome - ptosis and miosis
Restlessness/ agitation
More common in men 3: 1, and smokers. Alcohol may be a trigger. Fhx.
Screen mental health - suicidal thoughts are common due to excruciating nature of the pain
Triggers for cluster headaches?
Alcohol
Sublingual nitrates ( usually within an hour)
Disrupted circadian rhythm or during sleep
Strong smells - perfume or paint
Describe 4 different forms of aphasia and the region of the cortex affected
1) Wernicke’s aphasia - Comprehension of speech is impaired but able to form fluid speech. Due to lesion of superior temporal gyrus ( supplied typically by the inferior division of Left MCA). Wernickes area “ forms” speech before sending it to Broca’s area leading to sentences that make no sense, word substitution / neologisms “ word salad”.
2) Broca’s aphasia - Speech is non fluent and impaired. Lesion of the inferior frontal gyrus. Typically supplied by the left superior division of the MCA. Comprehension is normal but speech is non fluent, laboured, halting, repetition impaired.
3) Conduction aphasia - lesion affecting arcuate fasciculus the connection between Brocas and Wernickes
4) Global aphasia - large lesion affecting all Three of the above resulting in severe expressive and receptive aphasia.
Reflex roots:
Ankle
Knee
Biceps
Triceps
Dermatomes and nerve roots - revise ( Cheat sheet on answer card)
Vestibular schwannoma - pathophysiology
Originates from what?
BL usually indicates what condition ?
Key signs / classical history ?
IX
Vestibular schwannoma or acoustic neuroma - Benign tumour arising from the vestibular part of cranial nerve VIII ( Vestibulocochlear nerve). As tumour grows it compresses nearby structures including the trigeminal nerve and facial nerve.
originates from schwann cells in PNS providing myelin sheath around neurone.
Occur at the cerebellopontine angle sometimes called cerebellopontine angle tumours.
Acoustic neuromas are usually unilateral, bilateral acoustic neuromas are associated with neurofibromatosis type 11.
Presentation:
40 - 60 yrs with gradual onset of:
VEST
Vertigo
Ebsent corneal reflex
Sensorineural hearing loss
Tinnitus
cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy
IX: MRI of cerebellopontine angle & audiometry ( only 5% have normal audiogram)
Visual field defects: where is the lesion?
Homonymous hemianopia
Homonymous hemianopia with macular sparing
Homonymous quadrantopias - inferior vs superior
Bitemporal hemianopia 1) Upper quadrant > lower 2) lower quadrant > upper
Homonymous hemianopia - lesion of the opposite visual tract e.g. left homonymous hemianopia lesion of R optic tract.
Homonymous hemianopia with macular sparing - lesion of occipital cortex
Inferior quandrantopia - lesion of superior optic radiation - parietal
Superior quandrantopia - Lesion of inferior optic radiations in temporal lobe
( PITS pneumonic ( Parietal - Inferior, Temporal - superior)
Bitemporal hemianopia - lesion of optic chiasm.
Upper quadrant defect > lower quadrant defect - inferior chiasmal compression ( pituiatry tumour)
Lower quadrant defect > upper quadrant defect - superior chiasmal compression ( craniopharyngioma.
