Neurology Conditions Flashcards
What is the normal intracranial pressure in adults?
<15mmHg
How does raised ICP cause damage?
Compression of the brain leads to reduced blood supply to the cells –> Ischaemia –> No ATP –> Failure of NaKATPase –> Raised Na –> water follow –> cytotoxic cellular oedema
What investigations would you request if you suspect raised ICP?
CT head
Lumbar Puncture - IF SAFE (no evidence of coning) to get an opening pressure
Glucose, renal function, electrolytes, clotting
Toxicology screen
How does raised ICP present?
Headache Vomiting Change in consciousness Seizures Cushings reflex Changes to pupils Hemiparesis
What are the trio of signs seen in Cushing’s reflex?
Hypertension - sympathetic stimulation
Bradycardia - baroreceptors detect raised BP
Bradypnoea/ Cheyne-stokes breathing - Ischaemia to resp centre
What changes are seen to the eyes in raised ICP?
Pupils constrict initially then dilate
Peripheral visual field loss
Papilloedema and loss of venous pulsation at the disk
CN 3 and 6 palsy
What are the types of brain herniation?
Subfalcine/cingulate
Uncal
Tonsillar
What happens in a subfalcine/cingulate herniation and what does it cause?
Cingulate gyrus push under falx cerebri and compress anterior cerebral artery
- Contralateral weakness - especially leg
- Gait problems
What happens in an uncal herniation and what does it cause?
Uncus herniate through tentorial notch to compress:
CN3 = ipsilateral dilated, down and out
CN6 = diplopia when looking to side of lesion
Reticular formation - reduced GCS
Chemoreceptor trigger zone - N&V
Crus cerebri via kernohan’s notch - Ipsilateral hemiparesis
Ipsilateral PCA - contralateral homonymous hemianopia with macular sparing
What happens in a tonsillar herniation? What symptoms do you get?
Cerebellar tonsils herniate through foramen magnum leading to compression of brainstem.
Cardiorespiratory centres compressed - apnoea
Ataxia
CN6 palsy
Headache and neck stiffness
Flaccid paralysis
LOC
How are brain herniations managed?
Raise end of bed to 30 degrees IV Mannitol IV Dexamethasone Fluid restrict Normothermia Normoglycaemia Analgesia, sedation and anticonvulsants Decompressive craniectomy
What are the most common types of venous sinus thrombosis?
Sagittal sinus
Transverse sinus
How does sagittal sinus thrombosis present?
Headache - often sudden onset Vomiting Seizures Hemiplegia Decreased visual acuity Papilloedema
How does transverse sinus thrombosis present?
Headache - often sudden onset Mastoid pain Focal CNS signs Seizures Papilloedema
How does sigmoid sinus thrombosis present?
Cerebellar signs
How does inferior petrosal sinus thrombosis present?
CN5&6 palsy
Retro-orbital pain
What commonly causes cavernous sinus thrombosis?
Infection - facial pustules, folliculitis, sinusitis
How does cavernous sinus thrombosis present?
Headache Peri-orbital pain and oedema Proptosis Ophthalmoplegia - CN6 first, then 3 and 4 Central retinal vein thrombosis Hyperaesthesia of upper face (CN5)
What causes venous sinus thrombosis?
Hypercoaguable state - pregnancy, COCP, dehydration
Head injury
Tumours
Recent lumbar puncture
What are the differentials for venous sinus thrombosis?
Subarachnoid haemorrhage
Arterial infarct
Meningitis
Abscess
How is venous sinus thrombosis managed?
Anticoagulate - IV heparin or LMWH then warfarin
What are the complications associated with venous sinus thrombosis?
Transtentorial herniation due to mass effect or oedema
How would a venous sinus thrombosis appear on CT with contrast?
Empty delta sign - superior sagittal sinus should usually fill with contrast but doesn’t when thrombosed
What characteristics of a headache indicate it may be due to a space occupying lesion?
Worse on:
- Waking
- Lying down
- Bending forward
- Coughing
What symptom would mean space occupying lesions must be excluded as a cause?
Adult onset seizures - especially if aura (focal or localising) or post ictal weakness
What can cause a space occupying lesion?
Metastatic tumours - breast, lung, melanoma
Primary tumour - astrocytoma, glioblastoma, oligodendroglioma, meningioma
Aneurysm
Abscess
Chronic subdural haematoma
Granuloma
Cyst
What are the risk factors for idiopathic intracranial hypertension?
Obese
Female
30’s
COCP
Others - steroids, tetracyclines, vit A, lithium
How does idiopathic intracranial hypertension present?
Headache Narrowed visual fields Blurred vision and diplopia CN6 palsy Enlarged blind spot - papilloedema No change in cognition and consciousness
How is idiopathic intracranial hypertension managed?
Weight loss Acetazolamide or topiramate Prednisolone Optic nerve sheath fenestration (reduce pressure on optic nerve head) LP shunt
What is a hydrocephalus?
Excess volume of CSF fluid within ventricles due to imbalance of production and absorption
What are the types of hydrocephalus?
Obstructive/non communicating
Non-obstructive/communicating: CSF is free to flow but there is an imbalance of production and absorption
What can cause obstructive hydrocephalus?
Tumours
Congenital stenosis of the aqueduct
Haemorrhage of ventricles or subarachnoid space
What can be seen in an obstructive hydrocephalus?
Dilation of the ventricles superior to site
What can cause a non-obstructive hydrocephalus?
Increased production - choroid plexus tumour
Decreased absorption - meningitis, post-haemorrhagic
What investigations would you request for hydrocephalus?
CT - rule out differentials
LP - opening pressure and sample CSF
When mustn’t a lumbar puncture be carried out in a patient with a hydrocephalus?
If the cause is obstructive as the difference between pressures of the cranium and spine created by the LP will cause brain herniation
How does hydrocephalus present?
Signs of RICP i.e. headache worse on waking, lying down and Valsalva
How would hydrocephalus present in infants?
Increased head circumference - sutures not closed
Anterior fontanelle bulge
Sun set eye - can’t look up due to superior colliculus (midbrain) compression
What is the triad for normal pressure hydrocephalus?
Wet wacky wobbly
Urinary incontinence
Dementia
Disturbed gait - similar to parkinsons
What is a normal pressure hydrocephalus?
What is the appearance of the brain/ventricles?
Communicating hydrocephalus thought to be due to poor CSF absorption
Large ventricles (particularly 4th) but normal ICP
No substantial sulcal atrophy
What can cause a subarachnoid haemorrhage?
Traumatic or Spontaneous
Berry aneurysm rupture AV malformation Pituitary apoplexy Tumour invading blood vessels Idiopathic
How does a subarachnoid haemorrhage present?
Sudden onset thunderclap headache - occipital Vomiting Collapse, coma, seizure Meningism Terson's syndrome - vitreous haemorrhage
What are subarachnoid haemorrhages associated with?
Adult polycystic kidney disease
Ehlers danlos
Coarctation of the aorta
What can be seen on CT head in subarachnoid haemorrhages?
Hyperdense blood in:
Inter-hemispheric fissure
Sylvian fissues
Basal cistern
What arteries do berry anneurysms most commonly affect?
junction of anterior cerebral and anterior communicating
junction of middle cerebral and internal carotid
How are subarachnoid haemorrhages managed?
Bed rest, avoid straining, maintain BP
Nimodipine - 21 day to prevent vasospasm - cerebral ischaemia
Surgery - endovascular coiling, craniotomy and surgical clipping
What complications are subarachnoid haemorrhages associated with?
Rebleeding - 20%
Cerebral ischaemia - vasospasm
Hydrocephalus - blockage of arachnoid granulations
Hyponatraemia - SIADH
How would you investigate a suspected subarachnoid haemorrhage?
CT - very sensitive to timing so if suspicious do LP
LP
CT Angio
When would a lumbar puncture be carried out in suspected subarachnoid haemorrhage? What would the results be?
12 hours after headache
RBC start breaking down so sample will be xanthochromic (yellow) due to bilirubin
What causes a subdural haemorrhage? Therefore who do they most commonly affect?
Shearing forces on cortical bridging veins
Elderly and alcoholics (brain atrophy = taught bridging veins easier to rupture)
How does a subdural haematoma present?
Who would you see chronic subdurals in? How do they present on CT?
Slow onset of symptoms - RICP, upgoing planters etc.
Chronic subdural haematomas can be seen in infants and elderly
They are hypodense on CT
How would a subdural haematoma present on CT?
Crescent shaped hyperdense area + midline shift
What is the mechanism of getting an extradural haematoma?
What artery and what vein is commonly lacerated?
Acceleration Deceleration or Blow to side of head
Middle meningeal artery
Dural venous sinus
How does an extradural haematoma present?
Lucid interval followed by rapid deterioration
RICP
Upgoing plantars
Ipsilateral pupil dilation
How does an extradural haematoma appear on CT?
Biconvex hyper dense area
What is the pathophysiology of multiple sclerosis?
Chronic cell mediated autoimmune demyelination of the CNS
Attacks are separated in time and space (occur at multiple sites with remission in between)
What is the epidemiology of multiple sclerosis?
Mean age of onset = 30
Classically white women
Combination of genetic and environmental factors
How does multiple sclerosis commonly present initially?
Just one symptom - e.g. pain on eye movement with blurring of vision
Odd sensations such as wetness, burning or tingling
What systems are affected by multiple sclerosis?
Visual Mouth Urinary Digestive Sensory Muscular Throat - dysphagia Central
What are the visual manifestations of multiple sclerosis?
Nystagmus
Optic neuritis - common first presentation
Diplopia
What are the manifestations of multiple sclerosis seen in the mouth?
Difficulty swallowing
Slurring and stuttering of speech
What are the urinary manifestations of multiple sclerosis?
Frequency
Incontinence
What are the digestive manifestations of multiple sclerosis?
Sudden change in frequency
Constipation
Diarrhoea
What are the sensory manifestations of multiple sclerosis?
Increased sensitivity to pain
Tingling
Burning
Pins and needles
What are the muscular manifestations of multiple sclerosis?
Weakness
Cramping
Spasm
Lack of co-ordination - cerebellar involvement
What are the central manifestations of multiple sclerosis?
Fatigue
Depression
Cognitive impairment
Unstable mood
How can multiple sclerosis progress?
3 courses:
- Relapsing-remitting - complete remission between acute attacks
- secondary progression - relapsing remitting over time doesn’t fully remit
- Primary progression - progressive deterioration from onset
How is multiple sclerosis diagnosed?
MRI brain - demyelination plaques
MRI spine
CSF Electrophoresis - oligoclonal bands of IgG
Evoked potentials
What signs are seen in multiple sclerosis?
Lhermitte - electric shock in trunk and limb when neck flexed
Uhthoff’s - symptoms worse when warm
Pulfrich - Unequal eye latency - straight paths appear curved
How is multiple sclerosis managed?
Exercise, stop smoking, avoid stress
Acute relapses - IV methylprednisolone
Disease modifying drugs
Symtom control
What disease modifying drugs are used for multiple sclerosis?
Beta-interferon
Glatiramer
Dimethyl fumerate
Alemtuzimab
What drugs are used in symptom management for multiple sclerosis?
Baclofen - spasticity
Gabapentin - Oscillopsia and spasticity
Amantidine, CBT and mindfullness - fatigue
Urinary incontinence - normal meds
What is Parkinson’s disease?
Neurodegenerative disorder of the dopaminergic neurones in the pars compacta of the substantia nigra
Lewy bodies can be seen in the brainstem, cortex and basal ganglia
What triad of symptoms characterise Parkinson’s disease?
Bradykinesia
Hypertonia
Tremor
What symptoms are associated with Parkinson’s disease?
Asymmetrical symptoms
Bradykinesia - slow to move, shuffling short stepped gait, micrographia, reduced arm swing, microphonia
Hypertonia - leadpipe rigidity - combined with tremor = cogwheel
Resting tremor - 3-5Hz, pill rolling
REM sleep disorder, autonomic dysfunction, stooped posture, dementia/depression
What are the main differentials for Parkinson’s?
Benign essential tremor Huntington's Wilson's Lewy body dementia Psychogenic tremor
Parkinson’s plus - PSP, MSA, CBD
How is Parkinson’s diagnosed?
Clinical diagnosis based on core triad + response to treatment
Brain bank diagnostic criteria is used
Need to rule out differentials
What drug classes can be used to treat Parkinsons?
What important information should patients be given regarding their medication?
Don’t stop abruptly and be aware of malabsorption - neuroleptic malignant syndrome
Levodopa
Dopamine agonists - ropinirole
MAO-B Inhibitors - Rasagiline, selegiline
COM-T inhibitors - entacapone
What needs to be given alongside Levodopa and why?
What are the side effects of Levodopa?
Given with carbidopa to reduce peripheral breakdown
More motor complications and more negatives:
- Dyskinesia
- On off effect
- Dry mouth
- Palpitations
- Postural hypo
Give an example of a dopamine agonist?
What effect do they have on motor symptoms and motor side effects?
What are their side effects?
Ropinirole
Less effect on motor symptoms but fewer motor complications
Hallucinations and impulse control disorders
Ergot derived (bromocriptine) last resort as cause pulmonary, retroperitoneal and cardiac fibrosis
Describe the use of MAO-B inhibitors in Parkinson’s: Example and effect on motor symptoms/motor complications
Rasagiline
Fewer motor complications but reduced effectiveness
What other medications are used for other symptoms of Parkinson’s?
Sleepiness - Driving advice, modafinil
REM sleep disorder - melatonin, clonazepam
Postural hypo - fludrocortisone
Hallucinations - quetiapine and lorazepam
Dementia - cholinesterase inhibitor
Saliva drooling - SALT, glycopyronium
What is the prognosis of Parkinson’s and what are the main complications?
15 years
Aspirational pneumonia, bed sores, infection, poor nutrition, falls, contractures
What is Parkinsonism?
Other conditions which appear with similar symptoms to Parkinson’s but don’t have same cause
What are the main Parkinson’s plus disorders?
What else can cause Parkinsonism?
Progressive supranuclear palsy
Multiple system atrophy
Cortico-basal degeneration
Wilson’s, trauma, encephalitis
drugs (metoclopramide, haloperidol, chlorpromazine)
What symptoms would make you think a patient has progressive supra nuclear palsy?
postural instability - falling backwards
symmetrical
gaze palsies, speech and swallowing problems
What symptoms are characteristic of multiple system atrophy?
Early autonomic dysfunction - postural hypotension, urge incontinence, erectile dysfunction
cerebellar signs
pyramidal signs - UMN signs
What symptoms are associated with corticobasal degeneration?
Akinetic rigidity in 1 limb
Cortical sensory loss
Alien limb phenomenon
apraxia: difficulty in motor planning
What is motor neurone disease?
Neurodegenerative disease whereby there is selective loss of upper and lower motor neurones in the motor cortex, CN nuclei and anterior horn cells
NO SENSORY LOSS, no sphincter involvement or disturbance to eye movement
What are the types of motor neurone disease?
Amytophic lateral sclerosis
- loss in motor cortex and anterior horn cells
- typically UMN leg and LMN arm
Primary lateral sclerosis
- UMN
Progressive bulbar palsy
- affects brainstem motor nuclei (chewing, swallowing)
Progressive muscular atrophy
- LMN only typically progress from distal to proximal
How can motor neurone disease present?
Bulbar onset - slurred speech, swallow issues, tongue wasting
UL onset - weak grip, weak abduction, hand cramp, atrophy of hand muscles
LL onset - stumbling spastic gait, foot drop, thigh fasciculations, tibialis ant. wasting
Resp onset - dyspnoea, aspirational pneumonia, overnight hypoventilate
Frontotemporal dementia
How is motor neurone disease diagnosed?
Clinical diagnosis based on:
- UMN and LMN signs
- Disease progression
No other explanation
How would motor neurone disease be investigated?
Normal tests to rule out differentials - LP, B12, ACh antibodies
MRI - normal
EMG - large amplitude but long duration (therefore less action potentials)
Nerve conduction - normal motor conduction
What is the epidemiology of motor neurone disease?
2x more common in men
43-52
10% inherited and may present earlier
How is motor neurone disease managed?
MDT - palliative and end of life care
Speech - SALT, aids
Diet - modify diet/PEG
Breathing - physio, positive pressure ventilation, BiPAP
Cramps and spasms - baclofen, orthotics, exercises
Drooling - Hyoscine
Choking sensation - opiates
Riluzole can improve survival (only by months)
What are the main differentials for motor neurone disease?
!!Cervical spondylosis!! (LMN at level and UMN below) Benign fasciculations Myasthenia gravis Inclusion body myositis Multifocal motor neuropathy Lambert-eaton
What is the prognosis for motor neurone disease?
Median survival - 2-4 years
Most die in sleep - hypercapnia
What is bulbar palsy?
Result of diseases affecting CN 9-12
LMN lesions of tongue and muscles of articulation and swallowing
How does bulbar palsy present?
Bag of worms tongue - flaccid + fasciculations
Slurred speech (R is first to go)
Drooling
Raspy nasal voice
What is pseudobulbar palsy?
Bilateral UMN lesions of corticobulbar tracts (UMN of non-ocular cranial nerves)
How does pseudo bulbar palsy present?
Slow tongue movements= slow deliberate speech
Exaggerated jaw jerk
Absent palatal movements
Increased reflexes
!!No wasting or fasciculations as UMN
What can cause bulbar and pseudo bulbar palsy?
MND
Bulbar - polio, diphtheria, syringobulbia, infarct
Pseudobulbar - MS, stroke
What is bells palsy?
Acute, unilateral, idiopathic facial nerve palsy
What are the risk factors for developing Bells palsy?
20-40yo
Pregnancy
Diabetes
How does bells palsy present?
Forehead not wrinkled Eyeballs roll up Eyelid won't close Flat nasolabial fold Paralysis of lower face Ipsilateral post-auricular numbness or pain Reduced tase Hypersensitivity to sound Can't whistle Food trapped between gum and cheek Dry eyes
What are the main differentials for bells palsy? How would you rule these out/differentiate?
Ramsay hunt - ear pain proceded by palsy. Do VSV antibodies
Lyme disease - Can be bilateral. Do Borrelia antibodies
Facial nerve tumour and brainstem lesions - slow onset
Acoustic neuroma
How is bells palsy managed?
Oral prednisolone
Eye protection and lubricants
What complications are associated with bells palsy?
Exposure keratopathy and conjunctivitis
Synkinesis - misconnected links lead to unwanted facial movements (eye blink cause upturning of mouth)
Crocodile tears - cry when salivating
What are crocodile tears? (in reference to bells palsy)
Misconnection of parasympathetics mean unilateral lacrimation not salivation on eating
What is the prognosis for bells palsy?
By 6 months everyone have degree of recovery - if not consider alternate diagnosis
Incomplete paralysis without axonal degeneration - recover within weeks
Complete paralysis - 80% recover, 20 % start recovery later
What is myasthenia gravis?
Autoimmune disease where nicotinic acetylcholine receptors on the post-synaptic NMJ are blocked by antibodies
How does muscle fatigue progress in myasthenia gravis?
Extraocular Bulbar - swallow and chew Face Neck Limbs Trunk
How does myasthenia gravis present?
Ptosis - at night Diplopia Drooped mouth and snarl - when smiling Peek sign - eyelids separate on manual closure Voice fade on counting to 50 Unable to whistle
At what age do people commonly present with myasthenia gravis?
Women - child bearing
Men - 70’s
What investigations are requested for Myasthenia Gravis? What are the results?
Anti-ACh antibodies
Repetitive nerve stimulation shows reduced AP
CT thorax - thymoma
What can exacerbate myasthenia gravis?
Hypokalaemia
Infection
Change in climate, emotion or exercise
Drugs - Abx, Opiates, Beta blockers, lithium, phenytoin
What is myasthenia gravis associated with?
RA and SLE
Thymic hyperplasia
Thymic tumours
How is myasthenia gravis managed?
AChE inhibitors - pyridostigmine
Immunosuppression - prednisolone
Thymectomy
Trigger avoidance
What are the ADR’s associated with AChE inhibitors?
Lacrimation Salivation Sweating Vomiting Miosis
What is a myasthenic crisis?
Life threatening weakness of resp muscles
How can myasthenic crises be managed?
Intubate and ventilate
Plasma exchange
Immunosuppression and immunoglobulins
How could you differentiate between a myasthenic crisis and a cholinergic crisis?
Myasthenic: history of poor compliance. Good response to endrophonium challenge
Cholinergic (over medicated): Other cholinergic symptoms. Endrophonium challenge leads to fasciculations, miosis and worsening respiratory function
What is temporal arteritis?
Granulomatous vasculitis of medium and large sized vessels
Also known as giant cell arteritis
Who is commonly affected by temporal arteritis?
Women
>50
How does temporal arteritis present?
Rapid onset within <1 months
Headache - temporal/occipital
Jaw claudication
Vision changes (ant. ischaemic optic neuropathy) - amourosis fugax and visual disturbance Scalp tenderness Polymyalgia rheumatica symptoms - aching - morning stiffness (NOT WEAK) in proximal limbs Systemic symptoms - lethargic, depression, low grade fever
How would you investigate suspected temporal arteritis?
ESR - raised
CRP
Temporal artery biopsy - can get skip lesions so don’t ignore -ve biopsy
Temporal artery USS - halo sign, thickening and occlusion
How is temporal artery managed?
DONT DELAY High dose oral prednisolone - 4 weeks then taper \+ PPI, bisphosphonate and calcium Urgent ophthalm review Tocilizumab
If vision loss - IV methylprednisolone
What are the complications associated with temporal arteritis?
Irreversible bilateral vision loss - optic nerve ischaemia
Glucocorticoid related issues - diabetes, bone loss, infections
What are the types of neurofibromatosis?
Type 1 - von recklinghausen
Type 2
Both autosomal dominant
How does neurofibromatosis type 1 present?
Cafe-au-lait spots (within 1st year of life and increase) Freckling Neurofibromas - dermal, nodular Lisch nodules Short Macrocephaly Mild learning disability Optic gliomas
How does neurofibromatosis type 2 present?
Cafe-au-lait spots (fewer)
Bilateral vestibular schwannoma - sensorineural hearing loss, tinnitus, vertigo, compress local structures, RICP
Form of cataract
Meningiomas and gliomas
How are neurofibromatosis type 1 and 2 managed?
No cure
Remove symptomatic schwannoma
Annual hearing tests for type 2
What organisms commonly cause meningitis in adults?
Neisseria meningitidis
Strep pneumoniae
Listeria monocytogenes if immunocompromised
What investigations should be done if you suspect meningitis?
DONT DELAY TREATMENT
Lumbar puncture
Blood culture
PCR - neisseria
Blood gases
How would a lumbar puncture vary with the different causes for meningitis?
Bacterial - cloudy, low glucose, high protein, polymorphs
Viral - clear, normal glucose and protein, lymphocytes
Tuberculous - clear, low glucose, high protein, lymphocytes
How is meningitis managed in primary care?
Single dose benpen (ideally IV, likely IM) if non-blanching rash. If pen allergic no alternative
No rash - urgent hospital transfer, no empirical abx
How is viral meningitis managed?
Supportive
Present same as bacterial so usually follow that guidance
What is the general management for meningitis?
Blood cultures
IV ceftriaxone - empirical
Dexamethasone
Meningococci - ceftriaxone
Pneumococci - vancomycin + ceftriaxone
HiB - ceftriaxone
What are the main complications associated with meningitis?
Deafness - most common
Other neurological signs - epilepsy, paralysis
Infections - sepsis, intracerebral abscess
Pressure - brain herniation, hydrocephalus
What is prophylaxis is recommended for close contacts of those with meningitis?
Seek advice from regional health protection unit
Usually give prophylactic abx
What would indicate a CT head within an hour of arrival?
GCS <13 GCS<15 2hrs after injury Suspected open or depressed skull fracture Signs of basal skull fracture Post-traumatic seizure Focal neurological deficit More than 1 episode of vomiting
What would indicate the C spine needs immobilisation?
GCS <15 Neck pain or tenderness Focal neurological deficit Paraesthesia in extremities Any clinical suspicion of cervical spine injury
What should be done is GCS <8?
Call anaesthetist
Why is pain management important in head injury management?
Can lead to raised ICP
What would indicate a CT head within 8 hours?
Patient on warfarin
Some LOC or amnesia +
- Age 65 years or older
- Any history of bleeding or clotting disorders
- Dangerous mechanism of injury
- More than 30 mins retrograde amnesia of events immediately before injury
What is an epileptic seizure?
Transient occurrence of signs or symptoms due to abnormal electrical activity in the brain
Manifest as disturbance of consciousness, behaviour, emotion, motor function or sensation
What is epilepsy?
Disease of brain defined by:
- At least 2 unprovoked seizures more than 24hrs apart
- One unprovoked seizure with risk of 2nd within 10 years similar to those who have had 2
- Diagnosis of epilepsy syndrome
What are the risk factors for epilepsy?
Family history
Genetic condition associated - tuberous sclerosis or neurofibromatosis
Febrile seizures
Previous intracranial infections, brain trauma, surgery
Co-morbid conditions such as CVS disease or cerebral tumours
How is epilepsy assessed?
Check for risk factors Before, during, after event EEG Imaging Bloods
Urgently refer all people suspected of 1st seizure
What general advice would you give to people with epilepsy?
Try and record episodes Avoid driving, swimming and bathing Protect from injury Don't restrain seizing person Place in recovery position post seizure
What is the immediate management for epilepsy?
>5 mins - buccal midazolam or rectal diazepam IV lorazepam if access 2 doses of drug (5 mins apart) IV phenytoin if seizures continue Intubation and Rapid sequence induction
What is the general management for epilepsy?
Monotherapy
Different monotherapy
Dual therapy
Surgery or deep brain stimulation
When can anti-epileptic drug withdrawal be considered?
2-4 year seizure free
Gradually withdrawn over 2-3 months
What is the management for generalised seizures?
1st line - Valproate
2nd line - lamotrigine or carbemazepine
What is the management for focal seizures?
1st - carbemazepine (or lamotrigine)
2nd - Levetiracetam or valproate
What are the general ADR’s associated with anti-epileptic drugs?
Drowsiness Suicidal thoughts and behaviours Aggresion Hadaches Tremor Ataxia Gum hypertrophy Menstrual disturbance
What are the side effects of valproate and how is it monitored?
Osteoporosis, weight gain
LFT for months
FBC before starting
What are the side effects of carbamazepine and how is it monitored?
Rash, osteoporosis, SIADH, hyponatraemia, diplopia, enzyme inducer
Drug conc levels, FBC, LFT, U&E, GFT monitored
What are the side effects of phenytoin and how is it monitored?
Rash, osteoporosis, arrhythmia, raised ALP, low Ca and folic acid, BM affected, enzyme inducer
Drug conc levels and blood count monitored
What are the side effects of lamotrigine and how is it monitored?
Rash - inc. stephen johnsons, arrhythmia
Drug conc levels
What are the side effects of levetiracetam and how is it monitored?
Behaviour and mood changes
Risk of infection
What is subacute combined degeneration of the cord?
Dorsal and lateral columns affected by vitamin B12 deficiency
How does subacute combined degeneration of the cord present?
Joint position and vibration sense lost
Distal paraesthesia
UMN signs - typically legs - extensor plantars, brisk knee reflex, absent ankle reflex
How is subacute combined degeneration of the cord managed and what are the complications?
Vit B12
Stiffness and weakness persist
What are most cerebellopontine angle tumours?
Vestibular schwannomas
What is a classical history of a vestibular schwannoma?
Progressive changes
Vertigo
Hearing loss
Tinnitus
Absent corneal reflex
CNV, VII and VIII affected
How are cerebellopontine angle tumours investigated and managed?
MRI
Urgent ENT referral
Audiometry
Observe, give radio or do surgery
What is the prognosis of a cerebellopontine angle tumour?
Slow growing and benign
What are the borders of the cavernous sinus?
Roof - meningeal layer of dura
Medial - body of sphenoid
Floor - endosteal layer of dura
Lateral - meningeal layer of dura
What runs through the cavernous sinus?
CNIII CNIV CNV - 1 and 2 CNVI Internal carotid artery
Describe the epidemiology of a pituitary adenoma
Common - 10% of all people
Often never found or found incidentally
10% of all adult brain tumours
How can pituitary adenomas be classified?
Size - micro <1cm macro >1cm
Hormonal status
What investigations are done for pituitary adenomas?
Pituitary blood profile
Visual field test
MRI brain with contrast
Symptoms will depend on the hormones secreted and what it compresses
What are some differentials for pituitary adenomas?
Pituitary hyperplasia Craniopharyngioma Meningioma Brain mets Lymphoma Hypophysitis Vascular malformation
How are pituitary adenomas managed?
Hormone therapy
Surgery - transsphenoidal transnasal hypophysectomy
Radio
What pupil/eye changes would you see in a central herniation
fixed dilated pupils
sunset eyes - paralysed upward eye movement with pupil covered by lower lid
What is the contents of the cavernous sinus
Internal carotid artery
CN 3,4,6
Trigeminal nerve: ophthalmic and maxillary divisions
What is the first line investigation for ?venous thrombosis
MRI with venography
Describe the passage of CSF
Lateral ventricle foramen of monroe 3rd ventricle cerebral aqueduct 4th ventricle foramen of luschka/magendie
How does someone with myasthenic react to different types of neuromuscular blocking anaesthetic agents?
Increased sensitivity to non-depolarising (Rocuronium)
Reduced sensitivity to depolarising (Suxamethonium)
