NEUROLOGY Flashcards
What are the red flag symptoms for a patient presenting with a headache?
- Thunderclap - SAH
- Waking at night (+ weight loss + focal signs) = malignancy
- Fever w worsening headache, neck stiffness + rashes = meningism
- Scalp tender, visual changes, jaw claudication = GCA
- New-onset focal neurological deficits, personality change or cognitive decline = intracranial haemorrhage, stroke, SOL
- Headache that is posture dependent = raised ICP
- Headache associated with severe eye pain/blurred vision/N+V/red eye = AACG
What are the features of a migraine with NO aura?
- recurrent attacks lasting 4-72hrs
- unilateral
- fully reversible
- pulsating character
- nausea + photophobia
- pt prefers to be still in dark room
What are the features of a migraine with aura?
- 15-30mins aura followed by 1hr unilateral throbbing headache
Auras: - sparks in vision, blurring vision, lines across vision, lots of different visual fields
What is the acute management for a pt with a migraine?
- Oral triptan plus NSAID/paracetamol
- Consider nasal triptan in young people
- Prochlorperazine
When is the use of triptans contraindicated?
- IHD
- coronary spasm
- uncontrolled HTN
- SSRI use
When would you give prophylaxis for migraines? What do you give?
Offer to pts experiencing 2 or more migraines/month
- Propranolol (unless asthmatic)
- Topiramate (unless pregnant)
- Amitriptyline
How are tension headaches managed?
- Reassurance
- Basic analgesia
- Relaxation techniques
What is the acute management for cluster headaches?
- Triptans SC
2. High flow oxygen for 15-20 mins
What can be used as prophylaxis from cluster headaches?
- Verapamil
- Lithium
- Prednisolone (2-3 wks short course can break cycle)
What condition is commonly associated with giant cell arteritis?
Polymyalgia rheumatica
What is the gold standard test to diagnose GCA?
Temporal artery biopsy
- must be taken within 7 days of starting steroids
- skip lesions may be present
How do you manage GCA?
- High dose prednisolone - 6mg/day
- PPI + aspirin
- URGENT opthalmology r/v for pts with visual changes
What pre-hospital management can be given for suspected meningitis? (e.g. in primary care setting)
- if NO RASH present, transfer urgently to hospital with no Abx
- if rash present, give IM benzylpenicillin
What investigations should be performed in suspected meningitis?
- Bloods - U+E, FBC, LFT, glucose, coag screen, ABG, CRP
- Blood cultures + throat swab
- Whole blood PCR for N -meningitides
- LP - only if NO raised ICP signs
- CXR to r/o TB
- only perform CT head if reduced GCS or focal neurological signs
What is the treatment for pts presenting to hospital with suspected bacterial meningitis (over 3months age)?
Dexamethasone + ceftriaxone or cefotaxime
- tend to continue Abx for about 10 days
What Abx treatment is given to pts under 3 months presenting with bacterial meningitis?
cefotaxime + amoxicillin
- all those with bacterial meningitis should have hearing assessment within 4 months of discharge
What are the 3 branches of the trigeminal nerve?
V1 = ophthalmic V2 = maxillary V3 = mandibular
What are the main causes of trigeminal neuralgia?
Can be idiopathic
- MS can cause it
- Can be caused by compression by SOL = MRI is key to exclude this!!
How do you manage trigeminal neuralgia?
- Carbamazepine
- Refer to neuro if failed medical treatment or under 40
- Surgical decompression
What is the most common + severe cause of encephalitis? Name a few others also.
HSV-1
- others = echoviruses, VZV, EBV, coxsackie, mumps, measles, influenza
What investigations should be performed in a pt with suspected encephalitis?
- CSF - lymphocytosis, raised protein
- PCR for HSV
- CT head
- EEG
How is encephalitis managed?
- IV aciclovir for 2-3 weeks if HSV encephalitis
- Anticonvulsants if experiencing seizures
- Dexamethasone if features of raised ICP
What treatment can be used to help with hormonal headaches?
COCP
- hormonal headaches occur normally due to low oestrogen
What is cervical spondylosis? What are the typical symptoms?
Common condition caused by degenerative changes in cervical spine
- causes neck pain, usually made worse by movement BUT can often present with a headache
What are some risk factors for developing SAH?
- smoking
- HTN
- alcohol misuse
- cocaine use
- post-menopausal
- low oestrogen
- neurofibromatosis
- CTDs
What investigations should be performed in suspected SAH?
- CT head - blood will cause hyper attenuation in subarachnoid space
- LP - do if CT neg. Will have raised RCC (+ xanthochromia after 12hrs)
- Angiography used later to identify source of bleeding
How do you manage SAH?
IMMEDIATE NEUROSURGICAL REFERRAL
- Maintain cerebral perfusion
- Nifedipine given to reduce vascular spasm
- Endovascular coiling
What will the CT be like for an extradural haemorrhage?
They have a biconvex (lemon) shape, limited by cranial suture lines
How do you manage extradural haemorrhage?
- Reduce ICP
- 30 deg head tilt
- mannitol
- hyperventilate + sedation - Definitive management = craniotomy + evacuation of haematoma
What will the CT be like for subdural haemorrhage?
Crescent shaped (banana) - not limited by cranial suture lines
What are some arrhythmic causes of syncope?
- sick sinus syndrome
- 2nd degree AV block
- 3rd degree AV block
- dysfunctional pacemaker
- Supraventricular = AF, flutter, AVN re-entry tachycardia
- VT = more likely to cause syncope than SVT
What are some structural cardiogenic causes of syncope?
- Valvular disease e.g. aortic stenosis
- Cardiac masses e.g. atrial myxoma
- Cardiomyopathy e.g. HOCM
- Pericardial disease e.g. constrictive pericarditis
- Non-cardiac = PE, aortic dissection
What are red flag features of cardiogenic syncope which requires urgent CV assessment within 24hrs?
- ECG abnormality
- TLOC during exertion
- New/unexplained breathlessness
- Heart failure
- FHx of sudden cardiac death in those under 40y
- Presence of heart murmur
How do you manage AV node block if pt is unstable or risk of asystole?
Risk of asystole = mobitz type 2, complete heart block, prev asystole
1. IV Atropine 500mcg
If high risk of asystole:
- temporary transvenous cardiac pacing
- Permanent pacemaker
How do you manage a pt with VT who has (i) signs of shock (ii) haemodynamically stable?
(i) Immediate cardioversion is indicated if sBP under 90, chest pain, HF or syncope
(ii) Amiodarone, if this fails use cardioversion
What is the acute management for SVT?
- Vagal maneouvres
- IV adenosine
- Electrical cardioversion
What preventative management can be given to pts with SVT?
- Beta-blockers
2. Radio-frequency ablation
What are the 3 main causes of neurally mediated syncope?
- Vasovagal
- Situational syncope
- Carotid sinus hypersensitivity
What is carotid sinus hypersensitivity?
Syncope after manual manipulation of carotid sinus, which can happen accidentally whilst shaving, wearing a tight shirt collar or even certain head movements.
What are some causes of postural (orthostatic) syncope?
- Autonomic nervous failure secondary to drugs = most common cause
- Hypovolaemia
- Primary autonomic nervous disorder
- Secondary autonomic nervous disorder
With lying + standing BP, what is a significant drop in BP?
Drop of more than 20/10 mmHg within 3 mins of standing
What advice should you give for pts with postural syncope? What medical treatment can be used last line?
- Address cause
- Pt education re posture change, alcohol, heat + dehydration
- Raise head of bed, get up gradually
- BP monitoring
- Salt + water intake increased
- Medical treatment = fludrocortisone, midodrine
What clinical features are suggestive of epilepsy?
- attacks when lying down/sleeping
- aura before
- altered breathing, cyanosis
- obvious trigger e.g. TV
- tonic-clonic movements
- incontinent of urine, tongue biting
- prolonged post-ictal drowsy/confusion/amnesia
- transient focal paralysis (Todd’s palsy)
If seizure starts focally + then progresses to GTCS, what type of seizure is it?
Focal seizure
How are generalised tonic clonic seziures managed?
- Sodium valproate or lamotrigine
2. Carbamazepine or topiramate
What are the further classifications of focal seizures?
- Focal aware
- Focal unaware
- Awareness unknown
How are focal seizures managed?
- Carbamazepine
2. Sodium valproate or lamotrigine
What are absence seizures?
Usually in children
- pt becomes blank, stares in space + then abruptly returns to normal
- loss of awareness + unresponsive
- vacant expression for about 10seconds
Majority stop having once they get older
- treat with sodium valproate or ethosuximide
What are atonic seizures? How do you manage them?
DROP ATTACKS
- characterised by brief lapses in muscle tone usually last less than 3 mins
Management = sodium valproate then lamotrigine
What investigations should you perform in a patient with seizures?
- ABCDE, vitals, SaO2
- Neuro exam
- ECG
- EEG
- Blood glucose
- FBC to r/o infection
- U+E, bone profile - Na, Ca, Mg
- Toxicology screen
- Head CT
- Serum prolactin (doubled in GTCS)
- Serum CK (may be raised in GTCS)
What are some side effects of sodium valproate?
- teratogenic so avoid in women of child-bearing age
- liver damage/hepatitis/pancreatitis
- hair loss
- tremor
- increased appetite + weight gain
- nausea
- thrombocytopenia
- hyponatraemia
What are some examples of cytochrome P450 inducers? What effect shall they have on drugs metabolised by cytochrome p450?
CRAPS out drugs C - carbamazepine R - rifampicin A - barbituates (phenobarbitone) P - phenytoin S - St Johns Wort Others = chronic alcohol intake, smoking
- they reduce the concentration of drugs metabolised by cP450 system
What are some examples of cytochrome P450 inhibitors? What effect shall they have on drugs metabolised by cP450 system?
Some Certain Silly Compounds Annoyingly Inhibit Enzymes Grr
S - sodium valproate, SSRIs (fluoxetine, sertraline) C - ciprofloxacin S - sulphonamide C - cimetidine/omeprazole A - antifungals, amiodarone, allopurinol I - isoniazid E - erythromycin/clarithromycin G - grapefruit juice Others = acute alcohol intake
- increase concentration of drugs
What drugs are metabolised by the p450 system?
- warfarin
- COCP
- theophylline
- corticosteroids
- tricyclics
- pethidine
- statins
What is the definition of status epilepticus?
Seizure lasts longer than 5 mins or repeated seizures without intervening consciousness (more than 3 in 1hr)
How is status epilepticus managed in the (i) community (ii) secondary care?
(i) buccal midazolam or rectal diazepam
(ii) 1. Secure airway + high-flow O2
2. Assess CV + RS
3. Check BM
4. Gain IV access
5. IV Lorazepam 4mg - repeat after 10 mins if seizures persist
6. IV phenytoin if seizures persist - requires cardiac monitoring
What are some risk factors for stroke?
- HTN
- PVD
- hypercholesterolaemia
- AF
- smoking
- Hx of TIA
- Alcohol excess
- COCP
- DM
- Syphillis
- Heart disease
- Carotid bruit
- increased clotting e.g. Factor V Leiden
What are the features of a total anterior circulation stroke? Where does it occur?
ACA or MCA
All 3 of:
1. Unilateral weakness (and/or sensory loss) of face, arm + leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysplasia, visuospatial disorder)
What are the features of a partial anterior circulation stroke?
Cortical stroke in ACA or MCA
2 of the following:
1. Unilateral weakness (and/or sensory loss) of face, arm + leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysplasia, visuospatial disorder)
What are the features of a posterior circulation stroke?
At least 1 of:
- Cerebellar or brainstem syndrome
- LoC
- Ataxic hemiparesis
What are the features of Lacunar syndrome?
Subcortical stroke due to small vessel disease 1 of: 1. Unilateral weakness 2. Pure sensory stroke 3. Ataxic hemiparesis
What are the symptoms of a cerebellar stroke? (HINT: DANISH)
D - dysdiadokokinesia A - ataxia N - nystagmus I - intention tremor S - slurred speech H - hypotonia/hyporeflexia
- intense headache, N+V, vertigo
What does the NIHSS score do?
quantifies impairment caused by stroke
What investigations should you perform in suspected stroke?
- Non-contrast CT head - to r/o haemorrhage
- MRI - shows changes early in infarction + later, the extent of damage
- Bloods - r/o hypoglycaemia, infection + other stroke mimics, assess risk factors for stroke (cholesterol, clotting)
- ECG + 24h tape to look for arrhythmias
- Carotid artery doppler - look for carotid artery stenosis
What are some causes of ischaemic stroke?
- HTN - retinopathy? Nephropathy? Cardiomegaly?
- Cardiac source of Emboli - do echo + 48h tape
- Carotid artery stenosis - carotid USS or CT angio
- Hypo/hyper-glycaemia, dyslipidaemia, hyperhomocystinaemia
- Vasculitis - do ESR, ANA
- Prothrombotic states e.g. thombophilia, antiphospholipid syndrome
- Hyperviscocity e.g. polycythaemic, sickle cell
How do you immediately manage a suspected stroke?
- Admit to stroke unit?
- A-E assessment (remember to assess swallowing)
- CT head
- If CT rules out haemorrhage:
- thrombolysis (alteplase) if less than 4.5h since onset
- aspirin 300mg for 2 weeks - If haemorrhage present:
- refer to neurosurgery
- AVOID drugs that interfere with clotting - Stroke rehab with MDT
What secondary prevention is required post-ischaemic stroke?
- Clopidogrel 75mg OD
- Atorvastatin 80mg OD
- Carotid endarterectomy if stenosis over 70%
- Treat modifiable risk factors = HTN, lipids, smoking cessation, DM
- Anticoagulate if AF is cause
What are the causes of TIA?
- Atherothromboembolism from carotid artery is chief cause
- Cardioembolism - post-MI, AF, valve disease, prosthetic valves
- Hyperviscocity - polycythaemia, sickle cell, myeloma
- Vasculitis
What are some conditions which can mimic a TIA?
- syncope
- migraine
- retinal haemorrhage/detachment
- hypoglycaemia
- atypical seizure
- temporal arteritis
- labyrinthine disorders (present as vertigo + can be confused with posterior circulation TIA)
What investigations should be performed in a pt with suspected TIA?
Find cause + define vascular risk!
- FBC, U+E, ESR
- Glucose + lipids
- CXR
- ECG
- Carotid artery doppler + angiogram
- CT if high risk
- Echo
What is the ABCD2 score for assessing TIA? What does it compose of? How do you interpret the results?
Assesses 2-day risk of stroke. Pts with score of 4 or more should be seen by specialist within 24hrs. All others can be seen within 7 days
A - Aged over 60 (1)
B - BP 140/90mmHg and above (1)
C - Clinical features; unilateral weakness (2), speech disturbance without weakness (1)
D - Duration of symptoms; over 60 mins (2), 10-60mins (1)
D - Diabetes (1)
How do you manage pts post TIA?
- Control CV risk factors
- lower BP to below 140/85 mmHg
- 80mg atorvastatin
- help to stop smoking - Antiplatelets
- aspirin 300mg for 2 weeks
- clopidogrel 75mg OD - Carotid enderterectomy
- performed if at least 70% stenosis present
- perform within 2wks of first presentation
- do NOT stop aspirin during this time
What drugs can cause peripheral neuropathy?
- isoniazid
- amiodarone
- cisplatin
What type of disease is Guillain-Barre Syndrome?
Acute inflammatory demyelinating polyradiculopathy (AIDP)
What condition commonly precedes GBS?
2/3rds of patients will have a hx of gastroenteritis or flu-like symptoms in the preceding weeks
- associated with c. jejuni, CMV, EBV
What clinical features are present in GBS?
- Muscle weakness
- progressive symmetrical weakness
- affects lower limbs first
- moves from distal to proximal
- flaccid paralysis + areflexia
- maximal weakness reached in 4wks - Paraesthesias:
- pins + needles in legs + feet
- sensory abnormalities are mild - Areflexia - deep tendon reflexes lost. Plantars are downgoing
- Speech problems + facial weakness - may progress to cranial nerves
- Back + leg pain - prominent in children
- Respiratory distress
- dyspnoea on exertion + SOB
- 30% will require ventilation
What investigations are performed in suspected GBS?
- LP - raised protein + normal WCC
- Spirometry - reduced FVC
- Nerve conduction studies - slowed conduction velocity
- LFT - raised AST/ALT in 10-20%
How do you manage pts with GBS?
- IVIG + plasma exchange (plasmapheresis)
- Supportive treatment:
- respiratory = perform spirometry 6 hrly + ventilate if necessary
- cardiovascular = if dysautonomia present, insert Foley catheter
- DVT PROPHYLAXIS (PE is leading cause of death)
- pain management = gabapentin, carbamazepine
What are the classical clinical features of Charcot-Marie Tooth disease?
- high foot arches (pes cavus)
- weakness in hands
- distal muscle wasting causing ‘inverted champagne bottle legs’
- weakness in lower legs, particularly loss of dorsiflexion
- reduced muscle tone
- peripheral sensory loss
- steppage gait - foot hangs down causing toes to scrape ground = pt needs to lift leg higher than normal when walking
How is charcot-marie-tooth disease managed?
No treatment to alter underlying disease or to prevent it from progressing = Management is supportive from MDT
- neuro + geneticists to make diagnosis
- physio - maintain muscle strength + ROM
- OTs to assist ADLs
- Podiatrists assist with foot care + orthotics
- Orthopods correct disabling foot deformities
How do you differentiate between common peroneal nerve (L4-S1) palsy + tibial nerve palsy (L4-S3)?
In peroneal palsy there is weak ankle eversion
in tibial nerve palsy, you cannot invert the foot or flex toes
What are the clinical features of carpal tunnel syndrome?
- Aching pain in hand + arm, especially at night
- Paraesthesias in thumb, index + middle fingers, relieved by dangling hand over edge of bed + shaking it
- wasting of thenar eminence
What is (i) Phalen’s test (ii) Tinels test?
(i) Phalens = maximal wrist flexion for 1 min - induces pain of carpal tunnel
(ii) Tinels = tapping over median nerve ilicits symptoms
How is carpal tunnel syndrome managed?
- Splinting
- Steroid injection
- Decompression surgery
What are the key questions you should ask a pt who has presented with foot drop?
- Back pain - any radiation to leg?
- Leg numbness + tingling?
- Hx of trauma?
- Any change in activity prior to onset e.g. kneeling or crossing legs
What is the difference clinically between L5 root compression + common peroneal palsy?
L5 root compression: weak ankle dorsiflexion + eversion
- significant L5 compression will also cause S1 compression = ankle reflex is lost
Common peroneal nerve = ankle reflex is NOT los. Manage with foot drop splint
What is multiple sclerosis?
A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time + space
What are the typical features/presentation of MS?
- VISUAL
- optic neuritis
- optic atrophy
- B/L INO (weak adduction of ipsilateral eye, nystagmus of contralateral, convergence preserved)
- diploplia - SENSORY
- paraesthesias
- decreased vibration sense
- trigeminal neuralgia
- L’hermitte’s (paraethesia in limbs following neck flexion) - MOTOR
- spastic weakness (most commonly in legs)
- transverse myelitis - CEREBELLAR
- ataxia
- tremor - OTHERS
- swallowing disorders, constipation
- sexual dysfunction, urinary retention/incontinence
What is uhthoff’s phenomenon?
Transient worsening of vision when body gets overheated in hot weather, exercise, fever, saunas or hot tubs
How do you manage acute attacks of MS?
- IV methylprednisolone 1g/24h for 3-days
- does not influence long-term outcome but decreases duration + severity of attacks - Plasma exchange
What medication can be given to prevent relapses in MS?
- Interferons (IFN-B) - no role in primary progressive
- Monoclonal antibodies (natalizumab) - decreases relapses by 2/3 in RR
- Glatiramer - good for 2ndary progressive
What can polymyositis + dermatomyositis be associated with?
Malignancy
- lung
- breast
- ovarian
- gastric
What are the antibodies for polymyositis + dermatomyositis?
Polymyositis = anti-Jo-1 Dermatomyositis = Anti-Mi-2 and ANA
What are the typical clinical features of polymyositis?
- muscle pain, fatigue, weakness
- progressive, symmetrical proximal muscle weakness (shoulder or pelvic girdle)
- develops over weeks
- more common in females
What are the skin signs seen in dermatomyositis?
- Heliotope rash on eyelids
- macular rash (shawl sign over back + shoulders)
- Nailfold erythema
- Gottron’s papules on knuckles, elbows, knees
- Mechanics hands = painful, rough skin cracking of fingertips
- Retinopathy, haemorrhages, cotton wool spots
What are the extra-muscular features of dermatomyositis + polymyositis?
- fever
- arthritis
- bibasal pulmonary fibrosis
- Raynaud’s phenomenon
- Myocardial involvement = myocarditis or arrhythmias
What investigations are to be performed in poly/dermatomyositis?
- Muscle enzymes = raised CK, raised AST, ALT, LDH
- EMG
- Muscle biopsy provides definitive diagnosis
- Screen for MALIGANCY
- tumour markers, CXR, mammogram, pelvic/abdo USS, CT
Who is at risk of developing shingles?
Immunocompromised
- decline in immune function with advancing age
- chronic stress
- malignancy
- HIV, AIDS
- immunosuppressive therapy
- malnutrition
Who is given the shingles vaccine? Who can it NOT be given to + why?
Offered to all aged 70-79
- not given to those who are immunocompromised as it is a live vaccine given SC
What are the 4 types of motor neurone disease?
- Amyotrophic lateral sclerosis - most common
- UMN signs + LLMN fasciculations - Progressive Bulbar Palsy
- speech is quiet or nasal (donald-duck)
- MND, GBS, MG, central pontine myelinolysis all causes - Progressive Muscular Atrophy
- Primary lateral sclerosis
How is MND diagnosed?
Based on clinical findings + r/o other diagnoses
- MRI - r/o structural lesions
- LP - r/o inflammation
- EMG shows acute degeneration (reduced action potentials with increasing amplitude)
What drug can be used in MND to prolong life by about 3 months?
Riluzole
What is the prognosis of patients with MND?
most die within 3yrs
- of bronchopneumonia + respiratory failure
What conditions/ages are associated with development of myasthenia gravis?
Under 50yrs is more common in women + associate with other AI disease
Over 50 more common in men + associated with THYMOMA
What investigations should be performed in suspected MG?
- Antibodies = ACh-R antibodies, MuSK antibodies
- Tensilon test (rarely done anymore, give edrophonium IV + power will return within 1min)
- EMG - decreasing response to a train of impulses
- Reduced FVC
- Thymus CT
- TFTs
How do you manage myasthenic crisis?
IVIG or plasma exchange
- treat cause/trigger of relapse (usually respiratory tract infection)
How do you treat symptoms of MG?
pyridostigmine (anticholinesterase)
What are the different types of tremor? (RAPID)
- R - resting tremor
- goes on voluntary movement or distraction - A - Action/Postural
- absent at rest, worse on movement - I - Intention
- worse at end of movement (cerebellar damage) - D - Dystonic
What are the causes of an Action tremor? (BEATS)
B - benign essential tremor
E - endocrine = thyrotoxicosis, hypoglycaemia, phaeochromocytoma
A - Alcohol/caffeine/opioid withdrawal
T - Toxins (beta-agonists, theophylline, valproate)
S - Sympathetic (e.g. anxiety)
What is given to manage benign essential tremor?
- Propranolol
2. Primidone
What is multi-systems atrophy?
- early autonomic dysfunction = postural hypotension, bladder dysfunction
- cerebellar and pyramidal signs
- rigidity more than tremor
What is progressive supranuclear palsy?
- postural instability = falls
- speech disturbance (+ dementia)
- vertical gaze palsy
What is normal pressure hydrocephalus? How is it managed?
Triad of dementia, gait disorder + bladder instability
- enlarged ventricles on MRI + other signs of hydrocephalus
Management = Diagnostic LP + CSF removal, then VP shunt
What is the classical triad of Parksinsons?
- TREMOR
- resting tremor, 4-6Hz, pill-rolling - RIGIDITY
- lead-pipe rigidity, cog-wheel rigidity - BRADYKINESIA
- slow initiation of movement, reduction of amplitude on repetition
- monotonus voice
- micrographia
(GAIT = reduced arm swing, festinance, freezing)
What are the side effects of levodopa?
D - dyskinesia O - on-off phenomenon P - psychosis A - ABP reduced M - mouth dryness I - insomnia N - nausea + vomiting E - EDS (excessive daytime sleepiness)
If pts with PD have a relatively young onset + biologically fit, what treatment is given in PD?
- Dopamine agonists = ropinirole, pramipexole
- increased risk of hallucinations in elderly - MAO-B inhibitors = rasagiline, selegiline
- L-dopa = co-careldopa, co-beneldopa
- risk of gambling etc
If a patient is frail/has comorbidities, how do you treat their parkinson’s disease?
- L-dopa
2. MAO-B inhibs
What happens if patients suddenly stop taking dopamine agonists?
Neuroleptic malignant syndrome
- altered mental stare
- muscle rigidity
- autonomic instability
- hyperthermia
What is genetic anticipation? What disease is it seen in?
Feature of trinucleotide repeat disorders whereby successive generations have more repeats in gene, resulting in
- earlier age of onset
- increasing severity of disease
Occurs in Huntington’s chorea
What are some causes of vertigo? (IMBALANCE)
I - infection/injury (= labyrinthitis, Ramsay-Hunt, Trauma to petrous temporal bone)
M - Meniere’s disease
B - BPPV
A - Aminoglycosides
L - lymph
A - arterial = migraine or TIA/stroke
N - nerve = acoustic or vestibular Schwannoma
C - central lesions (demyelination, tumour, infarct)
E - epilepsy
What are important negatives for BPPV?
NO persistent vertigo (only lasts about a minute)
No speech/visual/motor/sensory disturbances
No tinnitus, headache, ataxia, facial numbness or dysphagia
What are the features you would suspect in a vestibular/acoustic neuroma?
Classic history of a combination of:
- vertigo
- hearing loss
- tinnitus
- absent corneal reflex
What is the gold standard investigation to diagnose acoustic neuroma?
MRI of cerebellopontine angle
What are the symptoms of Meniere’s disease?
- recurrent vertigo attacks lasting 2-4 hrs
- increasing aural fullness + tinnitus
- sensorineural hearing loss
- nystagmus always present
- positive Romberg’s test
What is the treatment of meniere’s disease?
- ENT assessment
- Acute attacks = prochlorperazine
- Prophylaxis = betahistine
- Inform DVLA (must stop driving until adequate symptom control achieved)
What are the features of vestibular neuronitis?
Often develops following viral infection e.g. URTI
- recurrent vertigo attacks lasting hours to days
- N+V
- horizontal nystagmus
NO HEARING LOSS OR TINNITUS
How is vestibular neuronitis managed?
Most are managed at home + tend to resolve themselves after 1 week
- may need prochlorperazine for acute episodes
- if persistent, long term rehab with vestibular exercises can be done (Cawthorne-Cooksey exercises)
What is the difference between vestibular neuronitis and labyrinthitis?
In labyrinthitis you will experience hearing loss
- there is no hearing loss in vestibular neuronitis
- treated the same
