Neurology Flashcards
Receptive aphasia aka..
Wernicke’s aphasia
Area of lesion in Wernicke’s (receptive) aphasia
Superior temporal gyrus
Blood supply to superior temporal gyrus
Inferior division of left MCA
Presentation of Wernicke’s aphasia
Sentences that make no sense, word substitution, and neologisms, but speech remains fluent - ‘word salad’
Comprehesion is impaired
Expressive aphasia aka…
Broca’s aphasia
Area of lesion in Broca’s aphasia
Inferior frontal gyrus
Blood supply to inferior frontal gyrus
Superior division of left MCA
Presentation of Broca’s aphasia
Speech non-fluent, laboured, halting
Repetition is impaired
Comprehension normal
Area of lesion in conduction aphasia
Arcuate fasiculus (connection between Wernicke’s and Broca’s area)
Presentation of conduction aphasia
Speech fluent but repetition poor, aware of errors
Comprehension normal
Location of lesion in global aphasia
Large lesion affecting all 3 areas (superior temporal gyrus, inferior frontal gyrus, arcuate fasiculus)
When should anti-epileptics be started following first seizure
- Neurological deficit
- Brain imaging shows structural abnormality
- EEG shows unequivocal epileptic activity
- Patient or their family/carers considers risk of having further seizure unacceptable
First line treatment generalised tonic-clonic seizures
Men - sodium valproate
Females - lamotrigine or levetiracetam
First line treatment focal seizures
Lamotrigine or levetiracetam
Second line treatment focal seizures
Carbamazepine, oxcarbazepine, zonisamide
First line treatment absence seizures
Ethosuximide
Second line treatment absence seizures
Male - sodium valproate
Female - lamotrigine or levetiracetam
Effect of carbamazepine in absence seizures
May exacerbate
First line treatment myoclonic seizures
Male - sodium valproate
Females - levetiracetam
First line treatment tonic or atonic seizures
Male - sodium valproate
Female - lamotrigine
CN I aka
Olfactory nerve
CN I function
Smell
CN II aka
Optic nerve
CN II function
Sight
CN III aka
Oculomotor nerve
CN III function
- Eye movement - medial rectus, inferior oblique, superior rectus, inferior rectus
- Pupil constriction
- Accommodation
- Eyelid opening
CN III palsy presentation
- Ptosis
- ‘Down and out’ eye
- Dilated, fixed pupil
CN IV aka
Trochlear
CN IV function
Eye movement - superior oblique
CN IV palsy presentation
Defective downward gaze → vertical diplopia
CN V aka
Trigeminal
CN V function
- Facial sensation
- Mastication
CN V lesion presentation
- Trigeminal neuralgia
- Loss of corneal reflex (afferent)
- Loss of facial sensation
- Paralysis of mastication muscles
- Deviation of jaw to weak side
CN VI aka
Abducens
CN VI function
Eye movement - lateral rectus
CN VI palsy presentation
Palsy results in defective abduction to horizontal diplopia
CN VII aka
Facial nerve
CN VII function
- Facial movement
- Taste to anterior 2/3 of tongue)
- Lacrimation
- Salivation
CN VII lesion presentation
- Flaccid paralysis of upper and lower face
- Loss of corneal reflex (efferent)
- Loss of taste
- Hyperacusis
CN VIII aka
Vestibulocochlear
CN VIII function
- Hearing
- Balance
CN VIII lesion presentation
- Hearing loss
- Vertigo
- Nystagmus
CN IX aka
Glossopharyngeal
CN IX function
- Taste to posterior 1/3 of tongue
- Salivation
- Swallowing
- Mediates input from carotid body and sinus
CN IX lesion presentation
- Hypersensitive carotid sinus reflex
- Loss of gag reflex (afferent)
CN X aka
Vagus
CN X function
- Phonation
- Swallowing
- Innervates viscera
CN X lesion presentation
- Deviated uvula from site of lesion
- Loss of gag reflex
CN XI aka
Accessory
CN XI function
Head and shoulder movement
CN XI lesion presentation
Weakness turning head to contralateral side
CN XII aka
Hypoglossal
CN XII function
Tongue movement
CN XII lesion presentation
Tongue deviates towards side of lesion
Afferent limb of corneal reflex
Opthalmic (division of trigeminal) nerve
Efferent limb of corneal reflex
Facial nerve
Afferent limb of jaw jerk reflex
Mandibular reflex
Efferent limb of jaw jerk reflex
Mandibular nerve
Afferent limb of gag reflex
Glossopharyngeal nerve
Efferent limb of gag reflex
Vagal nerve
Afferent limb of carotid sinus reflex
Glossopharyngeal nerve
Efferent limb of carotid sinus reflex
Vagal nerve
Afferent limb of pupillary light reflex
Optic nerve
Efferent limb of pupillary light reflex
Oculomotor nerve
Afferent limb of lacrimation reflex
Ophthalmic nerve
Efferent limb of lacimation reflex
Facial nerve
Anterior cerebral artery stroke features
- Contralateral hemiparesis and sensory loss
- Lower extremity > upper
Middle cerebral artery stroke features
- Contralateral hemiparesis and sensory loss
- Upper extremity > lower
- Contralateral homonymous hemianopia
- Aphasia
Posterior cerebral artery stroke features
- Contralateral homonymous hemianopia with macular sparing
- Visual agnosia
What arteries affected in Weber’s syndrome
Branches of posterior cerebral artery supplying the midbrain
Weber’s syndrome features
- Ipsilateral CN III palsy
- Contralateral weakness of upper and lower extremity
What arteries infected in Wallenberg syndrome (lateral medullary syndrome)
Posterior inferior cerebellar artery
Wallenberg (lateral medullary) syndrome features
Ipsilateral - facial pain and temperature loss
Contralateral - limb/torso pain and temperature loss
Ataxia
Nystagmus
Artery affected in lateral pontine syndrome
Anterior inferior cerebellar arteryF
Features of lateral pontine syndrome
Ipsilateral - facial pain and temperature loss, facial paralysis, deafness
Contralateral - limb/torso pain and temperature loss
Ataxia
Nystagmus
Retinal artery stroke features
Amaurosis fugax
Basilar artery stroke features
Locked in syndrome
Lacunar stroke features
Either isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia
Capgras syndrome
Delusion that friend or partner has been replaced by identical looking imposter
Othello syndrome
Irrational belief partner is having affair with no objective evidence
De clerambault syndrome
Delusional idea that person whom they consider to be of higher social and/or professional standing is in love with them
Cotard syndrome
Delusional idea one is dead
Examples 5-HT3 antagonists
Ondansetron
Palanostetron
Use 5-HT3 antagonists
Mainly management of chemotherapy related nausea
SEs 5HT3 receptor antagonists
Prolonged QT interval
Constipation
Advantage palanosetron over ondansetron
Reduced effect on QT interval
Inheritance ataxia telangiectasia
Autosomal recessive
When does ataxia telangiectasia present
Early childhood
Features ataxia telangiectasia
Cerebellar ataxia
Telangiectasia
IgA deficiency → recurrent chest infections
Malignancy and ataxia telangiectasia
10% risk of developing malignancy - lymphoma, leukaemia, non-lymphoid tumours
What is Bell’s palsy
Acute, unilateral, idiopathic facial nerve paralysis
Features Bell’s palsy
Lower motor neuron facial nerve palsy → forehead affected
Post-auricular pain
Altered taste
Dry eyes
Hyperacusis
Management Bells palsy
Oral pred within 72 hours of onset
?Antivirals if severe facial nerve palsy
Eye care - artificial tears, eye lubricants, tape eye closed at bedtime
Importance of eye care Bell’s palsy
Prevent exposure keratopathy
Referral criteria Bell’s palsy
If paralysis shows no signs of improvement after 3 weeks, refer urgently to ENT
When to consider referral to plastic surgery Bell’s palsy
For more long-standing weakness, e.g. several months
Prognosis Bell’s palsy
Most people make full recovery within 3-4 months
If untreated, around 15% of patients have permanent moderate to severe weakness
Causes brain abscess
- Extension of sepsis from middle ear or sinuses
- Trauma or surgery to scalp
- Penetrating head injuries
- Embolic events from endocarditis
Presentation brain asbcess
Depends on site of abscess, those in critical sites, e.g. motor cortex will present earlier
Headache
Fever (may be absent, usually not swinging)
Focal neurology
Nausea
Papilloedema
Seizures
Investigation brain abscess
CT scanning
Management brain abscess
Craniotomy and debridement of abscess
IV antibiotics
ICP management
Limitation of craniotomy and debridement of brain abscess
Abscess may reform because head is closed following drainage
IV antibiotics used in brain abscess
3rd gen cephalosporin + metronidazole
What is used for ICP management in brain abscess
Dexamethasone
Use of carbamazepine
Epilepsy, particularly partial seizures - most common use
Trigeminal neuralgia
Bipolar disorder
Adverse effects carbamazepine
P450 enzyme inducer
Dizziness and ataxia
Drowsiness
Headache
Visual disturbance, esp diplopia
Steven-Johnson syndrome
Leucopenia and agranulocytosis
Hyponatraemia secondary to SIADH
What is cataplexy
Sudden transient loss of muscular tone caused by strong emotion
What is Charcot-Marie-Tooth disease
Most common hereditary peripheral neuropathy, resulting in predominant motor loss
Management Charcot-Marie-Tooth disease
No cure, management focused on physical and occupational therapy
Features Charcot-Marie-Tooth disease
- Foot drop
- High arched feet
- Hammer toes
- Distal muscle weakness
- Distal muscle atrophy
- Hyporeflexia
- Stork leg deformity
May be history of frequently sprained ankles
Risk factors cluster headaches
Male
Smoker
Triggers cluster headaches
Alcohol
Noctural sleep
Features cluster headaches
Intense sharp, stabbing pain around one eye, each episode lasting 15 mins - 2 hours
Redness, lacrimation, and lid swelling
Nasal stuffiness
Miosis and ptosis in minority
How long do clusters last in cluster headaches
4-12 weeks
Occur around once a year
Investigations cluster headaches
MRI with gadolinium contrast - underlying brain lesions sometimes found
Referral cluster headaches
Should speak specalist advice from neurologist if patient develops cluster headaches
Acute management cluster headaches
100% oxygen
SC triptan
Prophylaxis cluster headaches
Verapamil
Treatment paroxysmal hemicrania
Indomethacin
What does sciatic nerve divide into
Tibial and common peroneal nerves
Where does injury to common peroneal nerve occur
Neck of fibula
Features common peroneal nerve
Foot drop
Weakness of foot dorsiflexion
Weakness of foot eversion
Weakness of extensor hallucis longus
Sensory loss over dorsum of foot and lower lateral part of leg
Wasting of anterior tibial and perioneal muscles
Risk factors degenerative cervical myelopathy
- Smoking
- Genetics
- Occupations exposing patients to high axial loading
Degenerative cervical myelopathy symptoms
Pain affecting neck, upper, or lower limbs
Loss of motor function - loss of digital dexterity, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence)
What is Hoffmans sign
Gently flicking one finger on a pateints hand → reflex twitching of other fingers on same hand
Suggests cervical myelopathy
Investigation degenerative cervical myelopathy
MRI of cervical spine
Findings MRI cervical spine in degenerative cervical myelopathy
Disc degeneration and ligament hypertrophy, with cord signal change
Referral degenerative cervical myelopathy
All patients need urgent referral for assessment by specialist spinal services (neurosurgery or ortho spinal)
Why is timing of surgery important in DCM
Any existing spinal cord damage can be permanent, early treatment (within 6 months of diagnosis) offers best chance of full recovery
Treatment DCM
Decompressive surgery
Role of observation in DCM
Close observation is option for mild stable disease
Role of physio in DCM
Should only be initiated by specialist services, as manipulation can cause more spinal cord damage
C2 dermatome landmark
Posterior half of skull (cap)
C3 dermatome landmark
High turtleneck shirt
C4 dermatome landmark
Low-collar shirt
C5 dermatome landmark
Ventral axial line of upper limb
C6 dermatome landmark
Thumb and index finger
C7 dermatome landmark
Middle finger and palm of hand
C8 dermatome landmark
Ring and little finger
T4 dermatome landmark
Nipples
T5 dermatome landmark
Inframammary fold
T6 dermatome landmark
Xiphoid process
T10 dermatome landmark
Umbilicus
L1 dermatome landmark
Inguinal ligament
L4 dermatome landmark
Knee caps
L5 dermatome landmark
Big toe, dorsum of foot
S1 dermatome landmark
Lateral foot, small toe
S2-3 dermatome landmark
Genitalia
Drugs causing peripheral neuropathy
Amiodarone
Isoniazid
Vincristine
Nitrofurantoin
Metronidazole
DVLA advice first unprovoked/isolated seizure
6 months off if no relevant structural abnormalities on brain imaging, and no definite epileptiform activity on EEG
If these conditions not met, 12 months
DVLA advice established epilepsy or multiple unprovoked seizures
May qualify for driving license if seizure free for 12 months
DVLA advice withdrawal of epilepsy medication
Should not drive whilst anti-epilepsy medication being withdrawn, and for 6 months after last dose
DVLA advice simple faint
No restriction
DVLA advice single episode syncope, explained and treated
4 weeks off
DVLA advice single episode unexplained syncope
6 months off driving
DVLA advice two or more episodes syncope
12 months off
DVLA advice stroke/TIA
1 month off, may not need to inform DVLA if no residual neurological deficit
DVLA advice multiple TIAs over short period of time
3 months off, inform DVLA
DVLA advice pituitary tumour
If craniotomy, 6 months
If trans-sphenoidal, can drive when no debarring residual impairment likely to affect safe driving
DVLA advice narcolepsy/cataplexy
Cease driving on diagnosis, can restart once satisfactory control of symptoms
DVLA advice chronic neurological disorders, e.g. MS, MND
Inform DVLA, complete PK1 form (application for driving license holders state of health)
Inheritance pattern dystrophinopathies
X linked recessive
DMD presentation
Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
Gower’s sign
30% have intellectual impairment
What is Gower’s sign
Child uses arms to stand up from squatted position
Beckers muscular dystrophy age of presentation
After 10 years
Features encephalitis
Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features, e.g. aphasia
Most common cause encephalitis
HSV-1 - 95% of cases in adults
Areas of brain affected in encephalitis
Temporal and inferior frontal lobes typically
CSF in encephalitis
Lymphoctosis
Elevated protein
Neuroimaging in encephalitis
Medial temporal and inferior frontal changes, e.g. petechial haemorrhages
Normal in 1/3
Best imaging modality in encephalitis
MRI
EEG in encephalitis
Lateralised periodic discharges at 2Hz
Management encephalitis
IV aciclovir
Features of temporal lobe seizures
May occur with or without impairment of consciousness
Aura in most patients
Typically last around one minute - automatisms, e.g. lip smacking/grabbing/plucking
Auras in temporal lobe seizures
Typically a rising epigastric sensation
Psychic or experiential phenomena, e.g. deja vu, jamais vu
Less commonly hallucinations - auditory, gustatory, olfactory
Features of frontal lobe seizures
Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march
Features of parietal lobe seizures
Paraesthesia
Features occipital lobe seizures
Floaters/flashes
Inheritance pattern essential tremor
Autosomal dominant
Essential tremor
Postural tremor, worse if arms outstretched
Improved by alcohol and rest
Affects upper limbs and titubation (head tremor)
Management essential tremot
Propanolol first line
Primidone sometimes used
What is supplied by the facial nerve
Face - muscles of expression
Ear - nerve to stapedius
Taste - anterior 2/3 of tongue
Tear - parasympathetic fibres to lacrimal glands, also salivary g lands
Causes of bilateral facial nerve palsy
Sarcoidosis
Guillain-Barre syndrome
Lyme diseae
Bilateral acoustic neuromas, e.g. in NF2
Bilateral Bells palsy
Difference between LMN and UMN facial nerve palsy
UMN spares upper face (forehead), LMN affects all facial muscles
Causes of LMN facial nerve palsy
Bell’s palsy
Ramsay-Hunt syndrome
Acoustic neuroma
Parotid tumours
HIV
MS
Diabetes mellitus
Causes of UMN facial nerve palsy
Stroke
MS
Inheritance Friedreich’s ataxia
Autosomal recessive
Genetic defect in Friedreich’s ataxia
Trinucleotide repeat disorder - GAA repeat in X25 gene on chromosome 25
What is unusual about Friedreich’s ataxia
It does not demonstrate anticipation
Age of onset Friedreich’s ataxia
10-15
Most common presenting features Friedreich’s ataxia
Gait ataxia
Kyphoscoliosis
Neurological features Friedreich’s ataxia
Absent ankle jerks/extensor plantars
Cerebellar ataxia
Optic atrophy
Spinocerebellar tract degeneration
Other features Friedreich’s ataxia
Hypertrophic obstructive cardiomyopathy (90%)
Diabetes mellitus
High arched palate
GCS motor scoring
6 - obeys commands
5 - localises to pain
4 - withdraws from pain
3 - abnormal flexion to pain
2 - extending to pain
1 - none
GCS verbal scoring
5 - orientated
4 - confused
3 - words
2 - sounds
1 - none
GCS eye scoring
4 - spontaneous
3 - to speech
2 - to pain
1 - none
What is Guillain-Barre syndrome
Immune-mediated demyelination of the peripheral nervous system often triggered by an infection
Infection classically triggering Guillian-Barre syndrome
Campylobacter jejuni
Antibody correlated with clinical features in Guillian-Barre syndrome
Anti-GM1
What is Miler Fisher syndrome
Variant of Guillain-Barre syndrome, associated with opthalmoplegia, areflexia, and ataxia. Eye muscles usually affected first
Guillain-Barre syndrome vs Miller Fisher syndrome
Guillain-Barre ascending paralysis, Miller Fisher syndrome descending paralysis
Antibody seen in Miller Fisher syndrome
Anti-GQ1b (90%)
Presentation Guillain-Barre
65% experience back/leg pain in initial stages of the illness
Progressive, symmetrical weakness of all limbs, classically ascending, reflexes reduced or absent, sensory symptoms mild with few sensory signs
Resp muscle weakness
Cranial nerve involvement (diplopia, bilateral facial nerve palsy, oropharyngeal weakness)
Autonomic involvement (urinary retention, diarrhoea)
Less commonly, papilloedema (secondary to reduced CSF resorption)
Investigations in Guillain-Barre syndrome
Lumbar puncture
Nerve conduction studies
LP findings Guillain-Barre syndrome
Rise in protein with normal WCC
Nerve conduction studies findings Guillain-Barre syndrome
Decreased motor nerve conduction velocity
Prolonged distal motor latency
Increased F wave latency
Features tension headache
Recurrent, non-disabling, bilateral headache, often described as tight-band
Features medication overuse headache
Present for 15 days or more per month
Developed or worsened whilst taking regular symptomatic medication
May be psychiatric co-morbidity
Highest risk medicines for medication overuse headache
Opioids
Triptans
Where in brain characteristically affected by herpes simplex encephalitis
Temporal (and inferior frontal) lobes
Features herpes simplex encephalitis
Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features, e.g. aphasia
Are peripheral lesions e.g. cold sores related to HSV encephalitis
No
CSF findings HSV encephalitis
Lymphocytosis
Elevated protein
CT findings HSV encephalitis
Medial temporal and inferior frontal changes, e.g. petechial haemorrhages
EEG pattern HSV encephalitis
Lateralised periodic discharges at 2Hz
Treatment HSV encephalitis
IV aciclovir
Inheritance pattern Huntington’s disease
Autosomal dominant
Genetic defect Huntington’s disease
Trinucleotide repeat disorder - repeat expansion of CAG
Pathophysiology Huntington’s disease
Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
Age of onset Huntington’s disease
35
Anticipation may be seen, where the disease presents at an earlier age in successive generations
Features Huntington’s disease
Chorea
Personality changes, e.g. irritability, apathy, depression
Intellectual impairment
Dystonia
Saccadic eye movements
Risk factors idiopathic intracranial hypertension
Obesity
Female
Pregnancy
Drugs
Drugs increasing risk of IIH
COCP
Steroids
Tetracyclines
Retinoids (isotretinoin, tretinoin), vitamin A
Lithium
Features IIH
Headache
Blurred vision
Papilloedema
Enlarged blind spot
6th nerve palsy may be present
Management IIH
Weight loss
Carbonic anhydrase inhibitors, e.g. acetazolamide
Topiramate
Repeated lumbar puncture for short term management
Surgery
Medications for weight loss in IIH
Semaglutide
Topiramate (particularly good as inhibits carbonic anhydrase)
For specialist consideration
Surgery IIH
Optic nerve sheath decompression and fenestration - prevent damage to optic nerve
Lumboperitoneal or ventriculoperitoneal shunt - reduce intracranial pressure
What is internuclear opthalmoplegia
Horizontal disconjugate eye movement due to a lesion in the medial longitudinal fasciculus
What is internuclear opthalmoplegia
Horizontal disconjugate eye movement due to a lesion in the medial longitudinal fasciculus
What is the role of the medial longitudinal fasciculus
Controls horizontal eye movements by interconnecting the 3rd, 4th, and 6th cranial nerve
Where is the medial longitudinal fasciculus located?
In the paramedian area of the midbrain and pons
Features internuclear opthalmoplegia
Impaired adduction of the eye on the same side as the lesion
Horizontal nystagmus of the abducting eye on the contralateral side
Causes internuclear opthalmoplegia
Multiple sclerosis
Vascular disease
Location of intracranial venous thrombosis
50% have isolated sagittal sinus thromboses
Remainder have co-existent lateral sinus thromboses and cavernous sinus thromboses
Features intracranial venous thrombosis
Headache, may be sudden onset
Nausea and vomiting
Reduced consciousness
Investigation intracranial venous thrombosis
MRI venography gold standard, CT venography alternative
D-dimer in intracranial venous thrombosis
May be elevated
Management intracranial venous thrombosis
Anticoagulation - typically low molecular weight heparin → warfarin for longer term anticoagulation
Presentation sagittal sinus thrombosis
May present with seizures and hemiplegia
Imaging findings sagittal sinus thrombosis
‘Empty delta sign’ on venography
Parasagittal biparietal or bifrontal haemorrhagic infarctions sometimes seen
Causes other than intracranial venous thrombosis of cavernous sinus syndrome
- Local infection, e.g. sinusitis
- Neoplasia
- Trauma
Features cavernous sinus thrombosis
Periorbital erythema and oedema
Opthalmoplegia - 6th nerve damage typically occurs before 3rd and 4th
Trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
Central retinal vein thrombosis
Features lateral sinus thrombosis
6th and 7th nerve palsies
What vessels involved in lacunar stroke
A single penetrating branch of a large cerebral artery
What structures affecting in lacunar stroke
- Internal capsule
- Thalamus
- Basal ganglia
Potential lacunar stroke syndromes
- Purely motor (most common)
- Purely sensory
- Sensorimotor stroke
- Ataxic hemiparesis
- Dysarthria-clumsy hand syndrome
Features ataxic hemiparesis caused by lacunar stroke
Ipsilateral weakness and limb ataxia that is out of proportion to motor deficit
What do lacunar strokes typically lack
Cortical findings, such as aphasia, agnosia, neglect, apraxia, or hemianopsia
Causes Lambert-Eaton syndrome
Small cell lung cancer (most common)
Breast cancer
Ovarian cancer
May occur independently as autoimmune disorder
Pathophysiology Lambert-Eaton syndrome
Antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system
Features Lambert-Eaton syndrome
- Repeated muscle contractions lead to increased muscle strength
- Limb-girdle weakness, affecting lower limbs first
- Hyporeflexia
- Autonomic symptoms - dry mouth, impotence, difficulty micturating
EMG findings Lambert-Eaton syndrome
Incremental response to repetitive electrical stimulation
Treatment Lambert-Eaton syndrome
Treatment of underlying cancer if present
Immunosuppression, e.g. pred and/or azathioprine
3,4-diaminopyridine
IV immunoglobulin
Plasma exchange
Lambert-Eaton syndrome vs myasthenia gravis
Muscle strength in Lambert-Eaton, weakness in MG
Opthalmoplegia and ptosis in MG, not LES
Use lamotrigine
Second line anti-epileptic for variety of generalised and partial seizures
Mechanism of action lamotrigine
Sodium channel blocker
Adverse effects lamotrigine
Stevens-Johnson syndrome
Complications meningitis
Sensorineural hearing loss (most common)
Seizures
Focal neurological deficit
Sepsis, intracerebral abscess
Brain herniation, hydrocephalus
Complications meningococcal meningitis
Waterhouse-Friderichsen syndrome
What is Waterhouse-Friderichsen syndrome
Adrenal insufficiency secondary to adrenal haemorrhage
Diagnostic criteria migraine
A - at least 5 attacks fulfilling B-D
B - headache lasting 4-72 hours
C - at least two of;
- unilateral location
- pulsating quality
- moderate or severe
- aggravation by/causing avoidance of routine activity
D - during headache, at least one of
- nausea/vomiting
- photophobia/phonophobia
E - not attributed to another disorder
Differences in migraines in children
- Shorter lasting
- More commonly bilateral
- GI disturbance
Migraine aura symptoms requiring investigation/referral
- Motor weakness
- Double vision
- Visual symptoms affecting only one eye
- Poor balance
- Decreased consciousness
First line acute treatment migraine
Combo therapy with;
- Oral triptan and NSAID, or
- Oral triptan and paracetamol
Acute migraine treatment in 12-17y/o
Nasal triptan rather than oral
Second line treatment acute mgiraine
Non-oral metaclopramide or prochlorperazine
Considering adding non-oral NSAID or triptan
Why caution in prescribing metaclopramide to young patients
Acute dystonic reactions may develop
When to give migraine prophylaxis
Migraine attacks having significant impact on quality of life and daily function, e.g. more than once a week on average, or prolonged and severe despite optimal acute treatment
First line options for migraine prophylaxis
Propanolol
Topiramate (not women of childbearing age)
Amitriptyline
Second line treatment migraine prophylaxis
Course of up to 10 sessions of acupuncture over 5-8 weeks
Treatment predictable menstrual migraine
Frovatriptan 2.5mg twice a day, or
Zolmitriptan 2.5mg BD-TDS
Specialist treatment options for migraine prophylaxis
Candesartan
Monoclonal antibodies directed against calcitonin gene-related peptipe receptor, e.g. erenumab
Use of pizotifen migraine prophylaxis
No longer recommended
What is multiple sclerosis
Chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS
Demographics MS
3x more common in women
20-40 years
Higher latitudes
Features relapsing remitting MS
Acute attacks (1-2 months) following by periods of remission
Features secondary progressive MS
Relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses
Gait and bladder disorders generally seen
Features primary progressive disease
Progressive deterioration from onset
More common in older people
Diagnostic criteria MS
Two or more relapses, and either;
- Objective clinical evidence of two or more lesions
- Objective clinical evidence of one lesion, together with reasonable historical evidence of an additional relapse
Visual features MS
- Optic neuritis
- Optic atrophy
- Uhthoff’s phenomenon
- Internuclear opthalmoplegia
What is Uhthoff’s phenomenon
Worsening of vision following rise in body temperature
Sensory features MS
- Pins/needles
- Numbness
- Trigeminal neuralgia
- Lhermitte’s syndrome
What is Lhermitte’s syndrome
Parasthesiae in limbs on neck flexion
Motor features MS
Spastic weakness - most commonly seen in legs
Cerebellar features MS
Ataxia
Tremor
Other features MS
Urinary incontinence
Sexual dysfunction
Intellectual deterioration
MRI findings MS
High signal T2 lesions
Periventricular plaques
Dawson fingers - hyperintense lesions penpendicular to the corpus callosum
CSF findings MS
Oligoclonal bands (and not in serum)
Increased intrathecal synthesis of IgG
Visual evoked potentials in MS
Delayed, but well preserved waveform
Management acute relapse MS
High dose steroids (oral or IV methylpred) may be given for up to 5 days
Action of steroids in acute relapse MS
Shorten the duration of relapse, but do not alter the degree of recovery
Indications for disease modifying drugs in MS
- Relapsing remitting disease + 2 relapses in the past 2 years + able to walk 100m unaided
- Secondary progressive disease + 2 relapses in the past 2 years + able to walk 10m (aided or unaided)
Disease modifying drug options MS
Natalizumab
Ocrelizumab
Fingolimod
Beta-interferon
Glatiramer acetate
Usual first line disease modifying drug MS
Natalizumab or ocrelizumab
Route of administration natalizumab
IV
Route of administration ocrelizumab
IV
Route of administration fingolimod
Oral formulations available
Route of administration beta-interferon
SC/IM
Route of administration glatiramer acetate
SC
What disease modifying drugs for MS considered less effective
Beta-interferon and glatiramer acetate
Treatment fatigue in MS
Once other problems, e.g. anaemia, thyroid, depression ruled out, trial amantadine
First line treatment spasticity MS
Baclofen
Gabapentin
Physio
Other options spasticity MS
Diazepam
Dantrolene
Tizanidine
Treatment bladder dysfunction in MS
Ultrasound to assess bladder emptying
If significant residual volume - intermittent self-catheterisation
If no significant residual volume - anticholinergics
What is oscillopsia
When visual fields appear to oscillate
Treatment oscillopsia MS
Gabapentin
Types of multiple system atrophy
MSA-P - predominant Parkinsonian features
MSA-C - predominant cerebellar features
Features multiple systems atrophy
Parkinsonism
Autonomic disturbance - erectile dysfunction, postural hypotension, atonic bladder
Cerebellar signs
Drugs exacerbating myasthenia gravis
Penicillamine
Quinidine
Procainamide
Beta-blockers
Lithium
Phenytoin
Gentamicin, macrolides, quinolones, tetracyclines
Age of onset myotonic dystrophy
20-30 years
Inheritance myotonic dystrophy
Autosomal dominant
Genetics myotonic dystrophy
Trinucleotide repeat disorder
Myotonic dystrophy DM1 vs DM2
Distal weakness more prominent in DM1
Proximal weakness more prominent DM2, severe congenital form not seen
Facial features myotonic dystrophy
Myotonic facies (long, haggard appearance)
Frontal balding
Bilateral ptosis
Cataracts
Dysarthria
Other features myotonic dystrophy
Myotonia (tonic spasm of muscle)
Weakness of arms and legs (distal initially)
Mild mental impairment
Diabetes mellitus
Testicular atrophy
Cardiac involvement - heart block, cardiomyopathy
Dysphagia
Inheritance neurofibromatosis
Autosomal dominant
Features neurofibromatosis type 1
Cafe-au-lait spots (≥6 15mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules)
Scoliosis
Phaeochromocytomas
Features neurofibromatosis type 2
Bilateral vesticular schwannomas
Multiple intracranial schwannomas, meningiomas, ependymomas
Drugs causing neuroleptic malignant syndrome
Antipsychotics
Dopaminergic drugs, e.g. levodopa (usually when stopped or suddenly reduced)
When does neuroleptic malignant syndrome occur
Usually hours to days of starting an antipsychotic
Features neuroleptic malignant syndrome
Pyrexia
Muscle rigidity
Autonomic lability - hypertension, tachycardia, tachypnoea
Agitated delirium with confusion
Bloods neuroleptic malignant syndrome
Raised AKI
AKI in severe cases
Leukocytosis
Management neuroleptic malignant syndrome
Stop antipsychotic
IV fluids
Dantrolene
First line treatment neuropathic pain
Amitriptyline
Duloxetine
Gabapentin
Pregabalin
Second line treatment neuropathic pain
Switch to one of the other first line drugs (not add)
‘Rescue therapy’ for exacerbations of neuropathic pain
Tramadol
Treatment localised neuropathic pain
Topical capsaicin
Causes normal pressure hydrocephalus
Reduced CSF absorption at arachnoid villi, may be secondary to head injury, SAH, or meningitis
Features normal pressure hydrocephalus
Urinary incontinence
Dementia and bradyphrenia (slowing of mental processes)
Gait abnormality
Timeline of symptom development normal pressure hydrocephalus
Develop over a few months
Imaging normal pressure hydrocephalus
Hydrocephalus with ventriculomegaly in absense of, or out of proportion to, sulcal enlargement
Management normal pressure hydrocephalus
Ventriculoperitoneal shunting
Complications VP shunt in normal pressure hydrocephalus
- Seizures
- Infection
- Intracerebral haemorrhages
Cause Parkinson’s disease
Degeneration of dopaminergic neurons in the substantia nigra
Features Parkinson’s disease
Bradykinesia
Tremor
Rigidity
Characteristic of symptoms in Parkinsons
Classically asymmetrical
Features of bradykinesia in Parkinson’s disease
Poverty of movement (hypokinesia)
Short, shuffling steps, reduced arm swing
Difficulty in initiating movement
Features of tremor in Parkinson’s disease
Most marked at rest, 3-5Hz
Worse when stressed or tired, improves with voluntary movement
Typically pill-rolling
Features of rigidity in Parkinsons disease
Lead pipe
Cogwheel - due to superimposed tremor
Other features of Parkinson’s disease
Mask like facies
Flexed posture
Micrographia
Drooling of saliva
Psychiatric features
Impaired olfaction
REM sleep behaviour disorder
Fatigue
Autonomic dysfunction - postural hypotension
Drug induced Parkinsonism vs Parkinson’s disease
Motor symptoms generally rapid onset and bilateral
Rigidity and rest tremor uncommon
Investigation Parkinsons disease
Diagnosis usually clinical
If difficulty differentiating between essential tremor and Parkinson’s disease, consider SPECT
First line treatment Parkinson’s disease
If motor symptoms affecting patients quality of life - levodopa
If motor symptoms not affecting patients quality of life - dopamine agonist, levodopa, or monoamine oxidase B
Levodopa vs dopamine agonists vs MAO-B inhibitors
Levodopa more improvement in motor symptoms. and ADL than dopamine agonists/MAO-B inhibitors
Levodopa more motor complications
Dopamine agonists greatest adverse effects
Treatment Parkinsons when continued symptoms despite optimal levodopa treatment, or developed dyskinesia
Add dopamine agonist, MAO-B inhibitor or COMT inhibitor
Dopamine agonists vs MAO-B inhibitors vs COMT inhibitors
Dopamine agonists most off-time reduction
COMT most adverse events, MAO-B least
Dopamine agonists most risk of hallucinations
Risk if Parkinsons medication not taken/not absorbed/drug holiday
Acute akinesia or neuroleptic malignant syndrome
Risk factors for impulse control disorders with Parkinsons medication
- Dopamine agonist therapy
- History of previous impulsive behaviours
- History of alcohol consumption and/or smoking
Management excessive daytime sleepines Parkinson’s disease
Adjust medications
Modafinil if alternative medications fail
Should not drive
Management orthostatic hypotension in Parkinson’s
Medication review
If symptoms persist, midodrine
Management drooling in Parkinsons
Glycopyrronium bromide
What medication is levodopa combined with
Decarboxylase inhibitor, e.g. carbidopa, benserazide
Why is levodopa combined with decarboxylase inhibitor
Prevents peripheral metabolism of levodopa to dopamine outside the brain, hence can reduce SEs
Common adverse effects levodopa
- Dry mouth
- Anorexia
- Palpitations
- Postural hypotension
- Psychosis
Adverse effects due to difficulty in achieving steady dose levodopa
- End of dose wearing off (symptoms worsen towards end of dosage interval → decline in motor activity)
- On-off phenomenon (large variations in motor performance
- Dyskinesias at peak dose - dystonia, chorea, athetosis
Management if patients unable to take levodopa orally
Dopamine agonist patch as rescue medication
Examples ergot derived dopamine receptor agonists
Bromociptine
Cabergline
Examples non-ergot derived dopamine receptor agonists
Ropinirole
Apomorphine
Adverse effects ergot-derived dopamine receptor agonists
Pulmonary, retroperitoneal, and cardiac fibrosis
Monitoring ergot-derived dopamine receptor agonists
Echo, ESR, creatinine and CXR obtained prior to treatment
Patients should be closely monitored
Other adverse effects dopamine receptor agonists
- Impulse control disorders
- Excessive daytime somnolence
- Hallucinations
- Nasal congestion
- Postural hypotension
Example MAO-B inhibitor
Selegiline
SEs amantidine
Ataxia
Slurred speech
Confusion
Dizziness
Lived reticularis
Examples COMT inhibitors
Entacapone
Tolcapone
Use of COMT inhibitors in Parkinsons
Used in conjunction with levodopa - COMT is enzyme involved in breakdown of dopamine
Use of antimuscarinics in Parkinsons
Now used more to treat drug-induced Parkinsonism rather than idiopathic Parkinson’s disease
Examples antimusarinics used in Parkinsons
Procyclidine
Benzotropine
Trihexyphenidyl
Causes of Parkinsonism
Parkinson’s disease
Drug induced, e.g. antipsychotics, metoclopramide
Progressive supranuclear palsy
Multiple systems atrophy
Wilson’s disease
Post-encephalitis
Dementia pugilistica
Toxins - carbon monoxide, MPTP
What causes dementia pugilistic
Chronic head trauma, e.g. boxing
Causes of peripheral neuropathy with predominantly motor loss
Guillain-Barre syndrome
Porphyria
Lead poisioning
Hereditary sensorimotor neuropathies, e.g. Charcot-Marie-Tooth
Chronic inflammatory demyelinating polyneuropathy
Diptheria
Causes of peripheral neuropathy causing predominantly sensory loss
Diabetes
Uraemia
Leprosy
Alcoholism
Vitamin B12 deficiency
Amyloidosis
Cause of alcohol neuropathy
Direct toxic effects of alcohol and reduced absorption of B vitamins
Alcohol neuropathy sensory vs motor symptoms
Sensory symptoms typically present prior to motor symptoms
How does vitamin B12 deficiency cause peripheral neuropathy
Subacute combined degeneration of the spinal cord
Order of presentation peripheral neuropathy secondary to vitamin B12 deficiency
Dorsal column usually affected first (joint position, vibration) prior to distal parenthesis
Effect of phenytoin on P450
Inducer
Acute SEs phenytoin
- Dizziness
- Diplopia
- Nystagmus
- Slurred speech
- Ataxia
- Confusion
- Seizures
Common chronic SEs phenytoin
- Gingival hyperplasia
- Hirsutism
- Coarsening of facial features
- Drowsiness
Other chronic SEs phenytoin
- Megaloblastic anaemia
- Peripheral neuropathy
- Enhanced vitamin D metabolism causing osteomalacia
- Lymphadenopathy
- Dyskinesia
Idiosyncratic SEs phenytoin
- Fever
- Rashes, inc severe reactions e.g. TEN
- Hepatitis
- Dupuytren’s contracture
- Aplastic anaemia
- Drug induced lupus
Teratogenic effects phenytoin
- Cleft palate
- CHD
Monitoring phenytoin
Check trough levels (immediately before dose) if;
- Adjustment of phenytoin dose
- Suspected toxicity
- Suspicion of non-adherence
Features progressive supranuclear palsy
- Postural instability and falls, stiff broad-based gait
- Impairment of vertical gaze - down gaze worse than up gaze
- Parkinsonism, bradykinesia prominent
- Cognitive impairment, primarily frontal lobe dysfunction
L-dopa in progressive supranuclear palsy
Poor response to L-dopa
Factors favouring psychogenic non-epileptic seizures
- Pelvic thrusting
- Family member with epilepsy
- Much more common in females
- Crying after seizure
- Don’t occur when alone
- Gradual onset
Factors favouring true epileptic seizures
- Tongue piting
- Raised serum prolactin
Roots of radial nerve
C5-T1
Muscle affected in injury to radial nerve at shoulder
Long head of triceps
Effect of injury to radial nerve at shoulder
Minor affects on shoulder stability in abduction
Muscle affected in injury to radial nerve at arm
Triceps
Effect of injury to radial nerve at arm
Loss of elbow extension
Muscle affected in injury to radial nerve at forearm
- Supinator
- Brachioradialis
- Extensor carpi radialis longus and brevis
Effect of injury to radial nerve at forearm
Weakening of supination of prone hand and elbow flexion in mid prine position
Sensory loss in radial nerve injury
Small area between dorsal aspect of 1st and 2nd metacarpals
Normal ICP when supine
7-15
What is the cerebral perfusion pressure
The net pressure gradient causing cerebral blood flow to the brain
How to calculate cerebral perfusion pressure
MAP - ICP
Causes raised ICP
- Idiopathic intracranial hypertension
- Traumatic head injuries
- Infection, e.g. meningitis
- Tumours
- Hydrocephalus
Features raised ICP
- Headache
- Vomiting
- Reduced level of consciousness
- Papilloedema
- Cushing’s triad
What is Cushing’s triad
- Widening pulse pressure
- Bradycardia
- Irregular breathing
Investigations raised ICP
- Neuroimaging (CT/MRI) to determine underlying cause
- Invasive ICP monitoring
Cut off for intervention in invasive ICP monitoring
> 20mmHg
Management raised ICP
- Treat underlying cause
- Head elevation to 30
- IV mannitol
- Controlled hyperventilation
- Removal of CSF
How does controlled hyperventilation help in raised ICP
Reduce pCO2 → vasoconstriction of cerebral arteries → reduced ICP
Limitation of controlled hyperventilation in raised ICP
- Temporary
- May reduce blood flow to already ischaemic parts of the brain
Methods for CSF removal
- Drain from intraventricular monitor
- Repeat LP
- VP shunt
Root of ankle reflex
S1-2
Root of knee reflex
L3-4
Root of biceps reflex
C5-6
Root of triceps reflex
C7-8
What is restless legs syndrome
Syndrome of spontaneous, continuous lower limb movements, may be associated with paresthesia
Features restless leg syndrome
- Uncontrollable urge to move legs - initially at night, but progress to occur during day, worse at rest
- Paresthesias, e.g. crawling or throbbing sensations
- Movements during sleep - periodic limb movements of sleep
Associations with restless leg syndrome
- Iron deficiency anaemia
- Uraemia
- Diabetes mellitus
- Pregnancy
Basic management restless legs syndrome
- Simple measures - walking, stretching, massaging affected limbs
- Treat any iron deficiency
First line drug treatment restless legs syndrome
Dopamine agonists, e.g. pramipexole, ropinorole
Other drug treatments restless legs syndrome
Benzodiazepines
Gabapentin
What is Reye’s syndrome
Severe progressive encephalopathy affecting children, accompanied by fatty infiltration of the liver, kidneys, and pancreas
Cause Reye’s syndrome
Unclear
Association with aspirin use
Potential viral cause
Peak incidence Reye’s syndrome
2 years
Features Reye’s syndrome
- Encephalopathy - confusion, seizures, cerebral oedema, coma
- Fatty infiltration of the liver, kidneys, and pancreas
- Hypoglycaemia
Managment Reye’s syndrome
Supportive
Roots sciatic nerve
L4-5, S1-3
What does sciatic nerve divided into
Tibial and common peroneal nerves
Muscles supplied by sciatic nerve
- Hamstrings
- Adductors
Motor features of sciatic nerve lesion
Paralysis of knee flexion and all movements below knee
Sensory features of sciatic nerve lesion
Loss below knee
Reflexes in sciatic nerve lesion
Ankle and plantar lost
Knee jerk in tact
Causes sciatic nerve lesion
- Fracture neck of femur
- Posterior hip dislocation
- Trauma
Teratogenic effects of sodium valproate
- Neural tube defects
- Neurodevelopmental delay
P450 and sodium valproate
P450 inhibitor
SEs sodium valproate
- Nausea
- Increased appetite and weight gain
- Alopecia
- Ataxia
- Tremor
- Hepatotoxicity
- Pancreatitis
- Thrombocytopenia
- Hyponatraemia
- Hyperammonaemic encephalopathy
Definition status epilepticus
Single seizure lasting >5 minutes
≥2 seizures within 5 min period without person returning to normal
First line treatment status epilepticus in pre-hosp setting
PR diazepam or buccal midazolam
First line treatment status epilepticus in hospital
IV lorazepam
Second line treatment status epilepticus in hospital
Repeat IV lorazepam after 5-10 mins
Third line treatment status epilepticus
Levetiracetam, phenytoin, or sodium valproate
Advantages levetiracetam as third line treatment for status
May be quicker to administer and have fewer adverse effects than other options
Fourth line treatment for status epilepticus, and when to give
Induction of general anaesthesia or phenobarb
If no response within 45 mins from onset - refractory status
Effect of stroke of anterior cerebral artery
Contralateral hemiparesis and sensory loss
Lower extremity>upper
Effect of stroke of middle cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Effect of stroke of posterior cerebral artery
- Contralateral homonymous hemianopia with macular sparing
- Visual agnosia
What artery is affected in Weber’s syndrome
Branches of posterior cerebral artery that supply the midbrain
Effect of stroke affecting branches of PCA supplying midbrain
- Ipsilateral CN III palsy
- Contralateral weakness of upper and lower extremity
What is lateral medullary syndrome
Stroke affecting posterior inferior cerebellar artery
Effect of stroke affecting posterior inferior cerebellar artery
- Ipsilateral facial pain and temp loss
- Contralateral limb/torso pain and temp loss
- Ataxia
- Nystagmus
What is lateral pontine syndrome
Stroke affecting inferior cerebellar artery
Effect of stroke affecting anterior inferior cerebellar artery
- Ipsilateral facial paralysis and deafness
- Contralateral limb/torso pain and temp loss
- Ataxia
- Nystagmus
Effect of stroke affecting retinal/opthalmic arteyr
Amaurosis fugax
Effect of stroke affecting basilar artery
Locked in syndrome
Common sites of lacunar strokes
Basal ganglia
Thalamus
Internal capsule
Criteria in Oxford Stroke Classification
- Unilateral hemiparesis and/or hemisensory loss of face, arm, and leg
- Homonymous hemianopia
- Higher cognitive dysfunction, e.g. dysphasia
What arteries does total anterior circulation infant involve
Middle and anterior cerebral artery
Oxford criteria and TACI
All 3 Oxford criteria present
What arteries does partial anterior circulation infarct involve
Smaller arteries of anterior circulation, e.g. upper or lower division of middle cerebral artery
Oxford criteria in PACI
2 Oxford criteria are present
What arteries involve in lacunar infarcts
Perforating arteries around internal capsule, thalamus, and basal ganglia
Presentation lacunar infarcts
One of;
- Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg, or all 3
- Pure sensory stroke
- Ataxic hemiparesis
What arteries involved in posterior circulation stroke
Vertebrobasilar arteries
Presentation posterior circulation stroke
1 of;
- Cerebellar or brainstem syndromes
- Loss of consciousnes
- Isolated homonymous hemianopia
Features suggesting more like haemorrhagic stroke
- Reduced consciousness level
- Headache
- N&V
- Seizures
Common management TIA
Aspirin 300mg immediately unless contraindicated
When is urgent admission indicated TIA
- More than 1 TIA (crescendo TIA)
- Suspected cardioembolic source
- Severe carotid stenosis
- Bleeding disorder or anticoagulant (imaging to r/o haemorrhage)
Management TIA within last 7 days
Assessment within 24 hours by stroke specialist
Management TIA over a week ago
Specialist assessment ASAP, within 7 days
Management haemorrhagic stroke
Neurosurgical review ?surgical intervention
Usually supportive - stop anticoag/antithrombotics, reversal
Lower BP
Management of BP in acute ischaemic stroke
Should not be lowered in acute phase unless complications,e .g. hypertensive encephalopathy, being considered for thrombolysis
Common management acute ischaemic stroke
Aspirin 300mg ASAP once haemorrhage excluded
Management of AF in ischaemic stroke
Should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days after onset
Management hypercholesterolaemia in stroke
If cholesterol >3.5, statin
Delay until at least 48 hours after due to risk of haemorrhagic transformatino
Criteria for thrombolysis in acute ischaemic stroke
- Can be administered within 4.5 hours of onset of stroke symptoms
- Imaging has excluded haemorrhage
When can thrombolysis be considered beyond 4.5 hours
If;
- Treatment can be started between 4.5 and 9 hours of known onset, or within 9 hours of the midpoint of sleep when they have woken with symptoms, and
- Evidence on CT/MR perfusion or MRI of the potential to salvage brain tissue
What agent should be used for stroke thrombolysis
Alteplase or tenecteplase
Alteplase if >4.5 hours
Should thrombolysis be performed if a patient is having thrombectomy
Yes
BP and thrombolysis
BP should be lowered to 185/110 before thrombolysis
Absolute contraindications to thrombolysis
- Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected SAH
- Stroke or TBI in prev 3 months
- LP in past 7 days
- GI haemorrhage in past 3 weeks
- Active bleeding
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg
Relative contraindications to thrombolysis
- Pregnancy
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery/trauma in prev 2 weeks
Which patients are eligible for thrombectomy
- Pre-stroke functional status of less than 3 on modified Rankin scale
- Score of more than 5 on National Institutes of Health Stroke Scale (NIHSS)
Timeline thrombectomy
Less than 6 hours
Offer if 6-24 hours from when last known well and imaging shows salvagable brain
Which arteries thrombectomy
Proximal anterior circulation
Consider if proximal posterior circulation (basilar of posterior cerebral artery) and imaging showing salvageable brain
Antiplatelet in secondary prevention of stroke
Clopidogrel
Aspirin if CI/not tolerated
When should carotid endarterectomy be considered in stroke
- Stroke or TIA in carotid territory
- Not severely disabled
- Stenosis >50%
Timeline carotid endarterectomy stroke
ASAP within 7 days
Cause subacute degeneration of spinal cord
- Vitamin B12 deficiency
- Recreational nitrous oxide inhalation (because it causes B12 def)
Structures affected in subacute degeneration of the spinal cord
- Dorsal column
- Lateral corticospinal tract
- Spinocerebellar tract
Features of subacute degeneration of the spinal cord due to dorsal column involvement
- Distal tingling/burning/sensory loss, symmetrical, legs>arms
- Impaired proprioception and vibration sense
Features of subacute degeneration of the spinal cord due to lateral corticospinal tract involvement
- Muscle weakness, hyperreflexia, spasticity
- Upper motor neuron signs
- Brisk knee reflexes
- Absent ankle jerks
- Extensor plantars
Features of subacute degeneration of the spinla cord due to spinocerebellar involvement
- Sensory ataxia → gait abnormalities
- Positive Romberg’s sign
What is syringomyelia
A collection of CSF in the spinal cord
What is syringobulbia
Fluid-filled cavity within medulla of brainstem
Causes syringomyelia
- Chiari malformation
- Trauma
- Tumours
- Idiopathic
Features syringomyelia
- Cape like (neck, shoulders, arms) loss of sensation to temp, but preservation of light touch, proprioception, and vibration
- Spastic weakness, predominantly lower limbs
- Neuropathic pain
- Upgoing plantars
- Autonomic features
- Horner’s syndrome
- Bladder and bowel dysfunction
Investigations syringomyelia
Full spine MRI - exclude tumour or tethered cord
Brain MRI - exclude Chiari malformation
Treatment syringomyelia
Treat cause of syrinx
If persistent or symptomatic, shunt into syrinx
Features third nerve palsy
- Eye is deviated ‘down and out’
- Ptosis
- Pupil may be dilated
Causes third nerve palsy
- Diabetes mellitus
- Vasculitis, e.g temporal arteritis, SLE
- Posterior communicating artery aneurysm
- Cavernous sinus thrombosis
- Weber’s syndrome
- Amyloid
- MS
When might third nerve palsy be a false localising sign
Uncal herniation through tentorium if raised ICP
TIA mimics
Hypoglycaemia
Intracranial haemorrhage
Role of CT brain in TIA
Should not be done unless clinical suspicion of alternative diagnosis that CT could detect, e.g. exclude haemorrhage
Role of MRI brain in TIA
- Determine territory of ischaemia
- Detect haemorrhage or alternative pathologies
Initial management TIA
Aspirin 300mg
Ongoing management TIA
Clopidogrel + aspirin (or ticagrelor) for 21 days, then clopi ongoing
Management TIA if not suitable for DAPT
Clopidogrel
Management AF in TIA
Anticoagulate as soon as haemorrhage excluded
Statin in TIA
High intensity statin, e.g. atorvastatin 20-80mg daily
Features of tremor in Parkinsonism
Resting pill rolling tremor
Features of tremor in essential tremor
Postural tremor, worse if arms outstretched
Improved by alcohol and rest
Titubation (nodding head movement)
Features of tremor in cerebellar disease
Intention tremor
Occurs with cerebellar signs, e.g. past-pointing, nystagmus
Features of trigeminal neuralgia
- Brief electric shock like pains, abrupt onset and termination, limited to one or more divisions of trigeminal nerve
- Pain commonly evoked by light touch
- Small areas in nasolabial fold or chin may be particularly susceptible (trigger areas)
- Main usually remit for variable periods
Red flags for serious underlying cause in trigeminal neuralgia
- Sensory changes
- Deafness or other ear problems
- History of skin or oral lesions that could spread perineurally
- Pain only in opthalmic division of trigeminal near (eye socker, forehead, nose) or bilaterally
- Optic neuritis
- FHx MS
- Age of onset before 40
Management trigeminal neuralgia
Carbamazepine first line
Referral trigeminal neuralgia
- Failure to respond to treatment
- Atypical feature
Adverse effects triptans
- Tingling
- Heat
- Tightness of throat and chest
- Heaviness
- Pressure
CIs triptans
History of or significant risk factors for IHD or CVD
Inheritance tuberous sclerosis
Autosomal dominant
Cutaneous features tuberous sclerosis
- Depigmented ash leaf spots which flouresce under UV light
- Shagreen patches - roughened patches of skin over lumbar spine
- Adenoma sebaceum (angiofibromas) - butterfly distribution over nose
- Subungal fibromata (under nails)
- Cafe-au-lait spots
Neurological features tuberous sclerosis
- Developmental delay
- Epilepsy
- Intellectual impairment
Other features tuberous sclerosis
- Retinal hamartomas (dense white areas on retina)
- Rhabdomyomas of heart
- Polycystic kidneys, renal angiomyolipomata
- Multiple lung cysts
Roots ulcer nerve
C8, T1
Sensory function ulnar nerve
Medial 1 1/2 fingers (palmar and dorsal)
Presentation ulnar nerve damage at wrist
- Claw hand
- Wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
- Wasting and paralysis of hypothenar muscles
- Sensory loss to medial 1 1/2 fingers
What is claw hand
Hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
Presentation ulnar nerve damage at elbow
- Claw hand (less severe than at wrist)
- Wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
- Wasting and paralysis of hypothenar muscles
- Sensory loss to medial 1 1/2 fingers
- Radial deviation of wrist
Presentation vestibular schwannoma (acoustic neuroma)
- Vertigo
- Unilateral sensorineural hearing loss
- Unilateral tinnitus
- Absent corneal reflex
- Facial palsy
Cause bilateral acoustic neuroma
Neurofibromatosis type 2
Investigation acoustic neuroma
MRI of cerebellopontine angle
Management acoustic neuroma
Surgery, radiotherapy, or observation
What causes homonymous hemianopia
Lesion of the opposite optic tract (e.g. left homonymous hemianopia = right optic tract)
What is an incongruous visual field defect
Incomplete or asymmetric visual loss
What does an incongruous visual field defect suggest
Optic tract lesion
What is a congruous visual field defect
Complete or symmetrical visual loss
What does a congruous visual field defect suggest
Optic radiation lesion or occipital cortex lesion
What does macula sparing suggest
Lesion of occipital cortex
Cause of superior homonymous quadrantanopia
Lesion of inferior optic radiations in temporal lobe (Meyer’s loop)
Cause of inferior homonymous quadrantanopia
Lesion of superior optic radiations in parietal lobe
Cause of bitemporal hemianopia
Lesion of optic chiasm
Cause of bitemporal hemianopia upper quad > lower quad
Inferior chiasmal compression, commonly pituitary tumour
Cause of bitemporal hemianopia lower quad > upper quad
Superior chiasmal compression, commonly craniopharyngioma
What is Wernicke’s encephalopathy
Neuropsych disorder caused by thiamine deficiency
Causes Wernicke’s encephalopathy
- Alcoholic (most common)
- Persistent vomiting
- Anorexia
- Stomach cancer
- Dietary deficiency
Features Wernicke’s encephalopathy
- Oculomotor dysfunction - nystagmus, ophthalmoplegia
- Gait ataxia
- Encephalopathy - confusion, disorientation, indifference, inattentiveness
- Peripheral sensory neuropathy
Opthalmoplegia in Wernicke’s encephalopathy
- Lateral rectus palsy
- Conjugate gaze palsy
Investigation Wernicke’s encephalopathy
- Red cell transketolase - reduced
- MRI
Treatment Wernicke’s encephalopathy
Urgent replacement of thiamine
Features Korsakoff syndrome
- Antero and retrograde amnesia
- Confabulation
