Neurology Flashcards
Epilepsy
- Definition + Classification
- Causes/Risk Factors
- Presentation
- Investigation
- Management
Definition + Classification
- Epileptic seizure = sudden synchronus fire of neurones. Epilepsy = ongoing liability to recurrent epileptic seizures.
- Classification of seizures based on: 1. where seizure begins 2. level of awareness during seizures 3. other features
Classification:
1. Focal (prev = partial) (unilateral)
- Awareness: Focal aware (simple partial); Focal unaware (complex partial) or Awareness unknown
- Other: Motor (e.g. Jacksonian March (spreads from hand to whole limb for example)); Non-motor (eg. deja vu, jamais vu), aura
- Focal seizures can cause: hallucinations (auditory, gustatory, olfactory), epigastric rising and automatisms (e.g. lip smacking)
-
Generalised (bilateral at onset)
- No Awareness/consciousness in any
- Other: Motor (eg. tonic-clonic), non-motor (eg. absence)
- Specifically: Tonic (stiffening), clonic (jerking), tonic-clonic (aka grand mal), absence (aka petit mal), atonic - Unknown onset
- Focal to bilateral seizure (prev secondary generalised seizure)
Causes/Risk Factors
- Primary generalised epilepsy/childhood epilepsy syndromes
- Focal lesions (->focal seizures) e.g. tumour, infarct, trauma, drugs, alcohol
Presentation
- Depends on seizure type
- Can be aura preceding
- Post-ictal confusion/headache
- Status (>5mins OR >2 seizures within 5 min period without return to normal in between)
- Good differentiators from syncope: long recovery, bitten tongue, pallor (syncope), cyanosis (seizure), stereotyped attack (seizure)
Investigation
- Bloods
- ECG (?long QT or arrhythmia)
- EEG - to diagnose + categorise (absence has characteristic 3Hz spike)
- MRI brain (r/o structural lesion)
Management
- Start anti-epileptics after 2nd seizure OR after 1st if neuro deficit, structural abnormality, EEG shows unequivocal epilepsy, risk of further seizure considered unacceptable
Generalised Tonic-Clonic
Males: Sodium Valproate
Females: Lamotrigine or Levetiracetam (no SV in child-bearing age)
Focal Seizures
1st: lamotrigine or levetiracetam
Absence
1st Ethosuximide
2nd: same as tonic-clonic
Myoclonic
Male: sodium valproate
female: levetiracetam
Tonic or Atonic
Male: sodium valproate
female: lamotrigine
Basically: all generalised (except absence) is males sodium valproate + female lamotrigine/levetiracetam. Absence = ethosuximide in both. Focal = lamotrigine/leveteracetam in both.
Give Examples of Epilepsy Syndromes that can occur in childhood
West Syndrome (3-12m) (infantile spasms)
Triad: infantile spasm, hypsarrhythmia on EEG, learning disabilty
Lennox-Gastaut (1-3yrs)
- multiple seizure types in sleep. Poor prog -> neurodevelopmental arrest/regression
Childhood Absence (4-12yrs)
- Good prog. 80% remit in adulthood.
Benign Rolandic Epilepsy (4-10yrs)
- most common childhood epilepsy
- Seizures at night, typically partial but can be secondarily generalised
- EEG = centro-temporal spikes
- V good prog, remits in adolescence
Status Epilepticus
Any one seizure >5 mins OR >2 seizures in 5 mins without full revovery in between.
How is it managed?
- A - Airway Adjunct
- B - O2
- C - resus as needed
- D - blood glucose
1. 5mins: IV lorazepam (or PR diazepam or buccal midazolam if no IV acess)
*IV 4mg lorazepam (0.05mg/kg up to max 4mg) *
Diazepam 10mg rectal or IV (adult dose, in children 1m-1y give 5mg, <1m = 2.5mg)
Buccal midaz 10mg (adult dose)
- 10mins:Repeat above (IV now if not before)
- 15mins IV phenytoin
- 45mins (refractory status) General Anaesthesia
Stroke
- Classification + Presentation
Ischaemic (85%)
- Subtypes: Thrombotic (large vessel), Embolic (small vessel, AF), TIA (resolves within 24h)
- RF: CVS RFs + AF
Haemorrhagic (15%)
Subtypes: Intracerebral or Subarachnoid
RFs:age, HTN, AV malformation, anticoag therapy
Oxford Stroke Classification
Looks at 3 criteria:
1. Unilateral hemiparesis and/or hemisensory loss of face, arm, leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction (eg. dysphagia)
Total anterior circulation (middlle + anterior cerebral arteries)
All 3 criteria
Partial anterior circulation (small arteries of ant. circ.)
2 of above criteria
Lacunar Infarct (internal capsule (passageway for all UMNs), thalamus (sensory passage), basal ganglia (control of body movement)
–> 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face, arm, leg or all 3
2. Pure sensory stroke
3. Ataxic hemiparesis
Posterior circulation stroke (vertebrobasiclar arteries)
–> 1 of the following:
1. Cerebellar or brainstem syndromes
(cerebllar = DANISH - dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia)
2. Loss of consciousness
3. Isolated homonymous hemianopia (if w/ other stuff –> ant. circ)
Where do the following arteries supply and how would stroke in this area therefore present?
Anterior circulation
- Anterior Cerebral Artery
- Middle Cerebral Artery
Posterior Circulation
- Posterior cerebral artery
- Cerebellar Artery
- Basilar Artery
Anterior Cerebral Artery
- Medial frontal lobes = motor homonculus (lower limbs) -> contralateral lower limb paralysis (flaccid then spastic)
- Medial parietal lobes = sensory homonculus (lower limbs) -> contralateral lower limb sensory loss (all modalities)
- Paracentral lobules = voluntary control of micturition –> incontinence
- Corpus callosum -> split-brain syndrome, alien hand
Middle Cerebral Artery **
- Lateral motor + sensory cortex –> contralateral motor/sensory upper limb/face (if prox to lenticulostriate arteries then lower limbs also affected due to internal capsule)
- Sup./Inf. optic radiations -> contralateral homonymous hemianopia
- Main trunk occlusion –> global aphasia (or broca’s (expressive) or wernickes (receptive) aphasia if only in branches to these bits)
- If dominant side (most = left) -> hemispatial neglect, tactile extinction, visual extinction, anosognosia (denile of any problem)
–> Malignant MCA (cerebral oedema + rise in ICP)
Posterior Cerebral Artery
- Posterior cerebral cortex –> contralateral homonymous hemianopia w/ macular sparing
Cerebellar Artery = crossed deficit
cerebellum -> ipsilateral signs
- DANISH (dysdiadochokinesia, ataxia (broad based), nystagmus, intention tremor, slurred speech, hypotonia)
prox lesion -> brainstem -> crossed-deficit
- CN nuclei damage = ipsilateral signs in face/eyes
- Ascending/descending tract damage = contralateral signs in rest of body (sensory cross on entering spinal cord, motor cross prior to desenct from brain)
Basilar Artery
If distal to pontine arteries
-> b/l occipital lobe infarct -> cortical blindness
-> B/L thalamic infarct ->sensory + LOC
Prox to pontine –> locked in syndrome (loss of all descending motor + CN 5 onwards)
How are strokes investigated and managed?
Investigation
1st: Non-contrast CT head
- Acute ischaemia: low density area (may take time to develop) or hyperdense artery sign (clot - visible immediately)
- Acute haemorrhage: hyperdense (blood) surrounded by hypodense oedema (immediately visible)
Management
Ischaemic (once haemorrhage ruled out w/ imaging)
- All: Aspirin 300mg (continued for 2/52)
- Thrombolysis (within 4.5h) AND Thrombectomy (within 6h) for Proximal Ant circulation stroke
- Thrombectomy alone (asap) if known to be well 6-24h previously (including wake-up stroke) AND confirmed prox ant circ stroke AND CT/MRI perfusion scanning shows potential to salvage brain tissue
- Also consider thrombectomy (+/- thrombolysis (4.5)) if known to be well 24h previously w/ proximal POCI (basilar or post cerebral artery) + potential to salvage tissue
Ongoing secondary prevention:
- 1st: 2/52 aspirin and clopidogrel life-long
- 2nd: aspirin + MR dipyramidole
TIA
- All: aspirin 300mg
- If within last 7 days –> assessment within 24h
- If >7d ago –> assessment within 7 days
- If >1TIA (crescendo) or suspected cardioembolic source or severe carotid stenosis -> discuss w/ stroke (?admission)
(no driving in all until seen by specialist)
N.B. if pt is on DOAC/warfarin/bleeding disorder w/ suspected TIA then need ED r/v + imaging prior to giving anything to make sure no bleed
At TIA review:
- MRI
- Urgent Carotid Doppler (?cartoid endarterectom if stenosis >70%)
Ongoing management
- 1st: Clopidogrel
- 2nd: aspirin + dipyramidole
Haemorrhagic
- neurological consultation. Mostly supportive w/ reversal of anticoagulation + BP control.
Other/General
- BP not lowered acutely unless complications e.g. Hypertensive encephalopthy
- Statins if cholesterol >3.5 (delay for 48h post-stroke to avoid haemorrhagic transformation)
AF
- Don’t start anticoag until haemorrhage is excluded AND not for 14d post-stroke
Presentation and management of the following types of headache
- Migraine
- Tension Headache
- Cluster Headache
- Trigeminal Neuralgia
- Temporal Arteritis
- Medication Overuse
- Idiopathic Intracranial Hypertension
Migraine
Diagnostic criteria = 5 attacks fulfilling following criteria:
1. Lasts 4-72h
2. 2 of following: unilateral, pulsating, mod-sev pain, causes avoidance of routine physical activity
3. During headache at least one: nausea/vomiting, photophobia/phonophobia
4. Not attributed to another disorder
+/- aura (scintillating scotoma, transient b/l hemianopic disturbance, sensory symptoms)
Management
Acute Attacks
- 1st: PO triptan + paracetamol/NSAID (12-17y nasal triptan instead)
Prophylaxis (if >2 attacks per month)
- 1st Propanolol or topiaramate (avoid topiramate in women of childbearing age)
- 2nd: Accupuncture
- other: riboflavin, if menstrual can give triptan as ‘mini prophylaxis’
Tension Headache
- Recurrent, non-disabling, b/l headache, ‘tight-band’
- simple analgesia
Cluster Headache
- men (3:1), smokers, alcohol can trigger
- pain 15mins -2h in clusters lasting 4-12w; intense sharp stabbing around one eye w/ red/watering/lid swelling, restlessness/agitation, nasal stuffiness
- Acute: 100% O2, SC triptan
- Prophylaxis: verapamil
- Specialist review (?neuroimaging)
Trigeminal Neuralgia
- Severe unilateral facial pain - like electric shocks, evoked by touch (washing, shaving, talking etc)
- most idiopathic BUT some can be due to compression of trigeminal root eg. tumour. Red flags: sensory change, deafness, hx of skin/oral lesions (can spread perineurally), pain only in ophthalmic division, bilateral pain, optic neuritis, fam hx of MS, onset <40yo (refer neuro)
- Mx: 1st: carbamazepine
Temporal Arteritis
- >60yo, rapid onset (<1/12), headache, jaw claudication, anterior iscahemic optic neuropathy (-> amarousis fugax + permanent visual loss), tender palpable temporal artery
- Big overlap w/ PMR
- Ix: raised ESR +/- CRP, biopsy (skip lesions)
- Tx: high dose steroids (PO pred (or IV methylpred if eye involvement) +ophthalmology r/v
- bone protection (long term steroids)
Medication Overuse
- >15dper month
- developed or worsened whilst taking regular analgesia (triptans + opioids = highest risk)
- wean overused meds, typically don’t use for >10d per month, can try preventatives e.g. propranolol, TCAs, CCBs etc.
Idiopathic Intracranial Hypertension
- RF: obesity, female, pregnancy, drugs: COCP, steroids, lithium
- Pres; headaches, blurred vision, papilloedema, enlarged blind spot, 6th CN palsy
- Mx - weight loss, acetazolamide, topiramate, repeated LP. ?optic nerve sheath decompression
Give headache Red Flags
- Infection: compromised immunity, worsening headache w/ fever
- Subarachnoid: sudden-onset reaching max intensity within 5 mins (thunderclap)
- Focal lesion: new-onset neuro deficit
- SOL: worse w/ cough, valsalva, sneeze, exercise, hx of malignancy, age <20
- Other: cognitive dysfunction, change in personality, impaired consciousness, recent head trauma, orthostatic headache (change w/ posture)
- Features of temporal arteritis or acute narrow angle glaucoma
- Substatial change in characteristics of headache
Describe the different types of aphasia
Fluent Speech
- Wernicke’s Aphasia (receptive) - fluent but doesn’t make sense. Comprehension impaired. - due to inferior division of left MCA lesion
- Conduction Aphasia (problem in arcuate fasciculus (connects Brocas+ Wernickes) - fluent w/ preserved comprehension but repetition is poor
Non-fluent Speech
- Broca’s Aphasia (expressive) frustrated, normal comprension, halting laboured speech - superior vision left MCA
- Global - large lesion affecting all 3 areas. May still be able to communicate w/ gestures.
What is the difference between Myasthenia Gravis and Lambert-Eaton Myasthenia Syndrome?
Myasthenia Gravis
- Path:autoimmune disorder -> destroys ACh receptors (Ab seen in 90%)
- Pres: muslce fatiguability –> diplopia, ptosis, prox muscle wekaness, dysphagia
- Associations: thymoma (15%), other autoimmune, thymic dysplasmia (60%)
- Ix- single fibre electromyography, CT to exclude thymoma, Ab to Ach receptors (in 90%, around 40% of the rest are +ve for anti-muscle-specific-tyrosine kinase ab)
- Mx:pyridostigmine (inhibits Ach esterase), immunosupression, thymectomy
- In crisis: plasmaphoresis, IV Ig
Lambert-Eaton Syndrome
Path: seen in small cell lung cancer (+ some breast/ovarian). OR independently as autoimmune condition.
Feat: limb girdle weakness (improves w/ use), hyporeflexia, autonomic sx (dry mouth, impotence, difficulty micturating)
Ix EMG
Mx - treat underlying Ca. Immunosupression (pred or azathioprine)
Guillain Barre Syndrome
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Immune mediated demyelination of PNS
- Triggered by infection (campylobacter)
Presentation
- Initial: leg/back pain
- Then progressive symmetrical weakness of all limbs (ascending, lower limbs first); hyporeflexia +/- slight distal paraesthesia (but mostly motor issue)
- Other: resp muscle weakness, CN involvement (-> diplopia, B/L facial nerve palsy, oropharyngeal weakness), autonomic (urinary retention, diarrhoea)
Investigations
- Lumbar puncture - high protein, normal WCC
- Nerve conduction studies (decresed motor nerve conduction (due to demyelination)
Management
- IV immunoglobulins
What are the side effects of phenytoin?
Acute
- Initial (sort of like a posterior stroke) –> dizziness, diplopia, nystagnum, slurred speech, ataxia
- Later: confusion, seizures
Chronic
- Gingivial Hyperplasia
- Hirsutism
- Coarse facial features
- Drowsiness
- Megaloblastic anaemia
- Peripheral neuropathy
Idiosyncratic
- Fever
- Rash (including TEN)
- hepatitis
- Dupuytren’s contracture
- aplastic anaemia
- drug-induced lupus (anti-histone antibodies)
Teratogenic -> cleft lip + congenital heart disease
Monitoring
- Monitor trough levels w/ dose adjustment, suspected toxicity or suspected non-adherence
Multiple Sclerosis
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Autoimmune demyelination of CNS
- Typically: women, age 20-40
Classification:
- Relapsing-Remitting (most common) (attacks 1-2/12 w/ remission in between)
- Secondary progressive (above but then start to get neuro problems between relapses (occurs within 15yrs in 65%))
- Primary progressive (10%) - progressive deterioration from onset
Presentation
- 2 or more relapses AND either objective clinical evidence of 2 or more lesions or one lesion w/ historical evidence of prev relapse
- General: Lethargy
- Visual: optic neuritis (common), optic atrophy, Uhthoff’s phenomenom (vision worses w/ rise in body temp)
- Sensory: paraesthesia, numbness, trigeminal neuralgia, Lhermitte’s (electric shock sensation in spine which spreads to limbs on neck flexion)
- Motor: spastic weakness (mostly legs)
- Cerebellar: ataxia, termor
- Other: incontinence, sexual dysfunction, intellectual deterioration
Management (no cure)
Acute Relapse:
- High dose steroids (PO or IV) 5d course (shortens relapse duration)
Ongoing - to reduce relapse rate
-1st: IV Natalizumab or ocrelizumab
- other: fingolimod, B-interferon, glatiramer acetate
Specific Symptom Management
*Fatigue *- Amantadine, mindfullness, CBT
Spasticity:
- 1st: baclofen and gabapentin
- 2nd: diazepam, dantrolene
- physio
Bladder dysfunction
- always USS to assess bladder emptying
- If significant reidual vol –>ISC
- If not –> anticholinergics
Oscillopsia - gabapentin
Cranial Nerves
What are they and what do they do? How would their lesions present?
CN I (Olfactory)
Smell –> loss of smell
CN II (Optic)
Sight –> visual loss
CNIII (Occulomotor)
Most eye movement (M/S/I rectus; inf oblique) –> Down + out eye (as only SO + LR still working)
Pupil constriction -> fixed dilated pupil
*Eyelid opening (LPS) -> ptosis
- Ischaemic damage (e.g. DM) can be pupil sparing whereas external compression in not
CN IV (trochlear)
*Eye movement (SO) *-> problems looking down –> diplopia (e.g. when going downstairs)
CN V (Trigeminal)
Facial sensation (3 branches - ophthalmic, maxillary, mandibular) -> neuralgia, loss of corneal reflex (afferent), loss of facial sesnsation
Muscles of mastication -> deviation of faw towards side of lesion
CN VI (Abducens)
Eye movement (LR) -> defective abduction -> horizontal diplopia
long course so can -> false localising lesions
CN VII (Facial)
Facial movement -> bells palsy (involves forehead)
*Anterior 2/3rd tongue *->loss of taste
Lacrimation
Efferent corneal reflex (orbicularis oculi) -> loss of reflex
Salivation –> dry mouth
Stapes stabilising muscle –> hyperacusis
Causes: LMN (eg. bell’s, ramsay-hunt, acoustic neuroma, partoid tumour/surgery, MS, DM) or UMN (stroke)
CN VIII (Vestibulocochlear)
hearing-> sensorineural hearing loss
Balance - > vertigo, nystagmus
N.B. acoustic neuromas = schwann cell tumour of cochlear nerve
CN IX (Glossopharyngeal)
Taste (post 1/3rd tongue-> reduced tast
Salivation
Swallow
Afferent gag reflex -> loss of reflex
Mediates input from carotid body -> hypersensitive
CN X (Vagus)
Phonation
Swallowing - loss of efferent gag, uvular away from site of lesion
Innervates viscera
CN XI (Accessory)
Head and shoulder movement - weakness truning head to contralateral side
CN XII (hypoglossal)
Tongue movement - deviates towards lesion
Bell’s Palsy
What causes it?
How does it present?
How is it managed?
Cause
- Unknown ?HSV
- Peak 20-40y + more common in pregnancy
Presentation
- Lower motor neurone facial palsy - NOT forehead sparcing
- Also: hyperacusis, altered taste, dry eyes (lose efferent corneal reflex)
- can have post-auricular pain preceding
Management
- PO pred within 72h (generally NOT recommended to give anti-virals but ?some role in severe palsy - needs specialist discussion first)
- Eye care (to prevent exposure keratopathy) (eye taping, artificial tears/lubricant)
Follow up
- If no improvement at 3/52 then urgent ENT referral
Prognosis
- most make full recovery in 3-4/12
Neuroleptic Malignant Syndrome
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
- Cause: Antipsychotic meds (typical + atypical), dopaminergic drugs (eg. levodopa)
- Mortality of 10%
Presentation
- within hours-days of starting the drug
- Pyrexia, muscle rigidity, autonomic lability (HTN, tachycardia + tachypnoea), agitated deliriu, confusion
Investigation
- Raised CK
- AKI secondary to rhabdomyolysis (if severe)
- +/- leucocytosis
Management
- Stop antipsychotic
- Often need ITU supportive management - IVI +/- dantrolene, bromocriptine
Motor Neuron Disease
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- unknown cause
- Can present w/ upper or lower motor neuron signs
- Typically >40yo
Presentation
Typically:
- Fasiculations
- Mixture or upper + lower motor neurone signs
Upper: hyertonia, hyperreflexia, weakness/paralysis
Lower: weakness/paralysis, hypotonia, hyporeflexia, rapid muscle wasting, fasiculation
- Wasting of small hand muscles is common
- Absence of sensory signs, external ocular muscle involvement or cerebellar signs
Patterns
- Amyotrophic Lateral Sclerosis - simultaneous upper/lower motor neuron involvement, starts in one limb then spreads to others + trunk w/ relentless progression
- Progressive musclar atrophy - pure LMN - weakness, wasting, fasiculations
- Bulbar palsy - lower CNs -> dysarthria, dysphagia (worse w/ liquids than solids), tongue fasiculation w/ slow movement, emotional incontinence + pathological laughter (pseudobulbar)
Investigation
- Clinical diagnosis, no diagnostic test
Management
- Riluzole (used in Amyotrophic lateral sclerosis)
- Resp care: NIV (BiPAP at night)
- Nutrition: initially smaller meals, then make consistency more liquid, then PEG feeding (NG not suitable as only used for 4-6/52 due to risk of ulceration)
poor prognosis w/ most dead in 3 years
Degenerative Cervical Myelopathy
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- A collection of pathological conditions –> progressive cervical cord compression + dysfunction
- RFs: smoking, lumbar spinal stenosis, genetics, occupations w/ high axial load
Presentation
- Early = subtle sx.
- Pain (neck, upper or lower limbs)
- Loss of motor function (digital dexterity esp affected; or arm/leg weakness/stiffness -> impaired gait)
- Loss of sensory function
- Loss of autonomic (urinary or faecal incontinence or impotence)
- Hoffmann’s sign- flick distal phalanx of middle finger and thumb/1st finger will adduct
Investigation
- MRI cervical spine (can show disc degen, ligament hypertrophy + cord signal changes)
Management
- Spinal surgery (best if within 6/12 of diagnosis) (post-op sx can recur at adjacent spinal levels -need to monitor)
- (physio must be done by specialist services as otherwise may worsen symptoms)
Encephalitis
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
- HSV1 = 95% of cases
- Typically temporal + inferior frontal lobes
- (herpes simplex tends to affect temporal lobe -> aphasia)
Presentation
- Fever, headache, pscych symptoms, seizures vomiting, ataxia, aphasia
- but no meningisim
Investigation
- CSF: lymphocytes, protein, PCR for HSV, VZV + enteroviruses
- MRI: normal in 33% of patients. Can also see: petechial haemorrhages, swelling + increased brain signal (esp in temporal + inferior frontal lobes)
- EEG - periodic discharges at 2Hz
Management
- IV aciclovir
Essential Tremor
Give features and management
Features
- Autosomal dominant
- Postural tremor (worse w/ outstretched arms), can also -> head titubation/tremor
- Improved by: alcohol + rest
Management
Propanolol
Parkinson’s Disease
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Degeneration substantia nigra
- Other causes of parkinsonism: drug-induced (antipsychotics, metoclopramide), wilson’s, progressive supranuclear palsy, multiple system atrophy
Presentation
- Triad: Bradykinesia, Tremor (pill-rolling, resting, 3-5Hz), Rigidity (cog-wheel/leadpipe) - typically asymmetrical (BUT in drug-induced can be b/l)
- Other: mask-like face, depression, dementia, micrographia, anosmia, REM sleep disorder, autonomic dysfunction
Investigation
- Clinical diagnosis in most
- Or SPECT if needing to distinguish between PD and Essential tremor
- (diagnosis + management done in secondary care)
Management
First Line:
- If motor sx affecting QOL: Levodopa
- If motor sx not affecting QOL: Dopamine agonist, levodopa or MAO-B inhibitors
- SEs: impulse control disorder, sleepiness, hallucinations
Specifics about drugs:
- Levodopa is combined w/ decarboxylase inhibitor (e.g.carbidopa) to prevent peripheral conversion to dopamine + reduce SEs. Side effects can occur due to difficulty in acheiving steady state e.g. end-of-dose wearing off, on-off phenomenon, dyskinesias at peak dose (dystonia, chorea, athetosis). Becomes less effective over time *If stopped acutely –> acute dystonia *
- Dopamine receptor agonists eg. bromocriptine, ropinirole, cabergoline. Can -> pulm + retroperitoneal fibrosis.
- MAOB e.g. selegiline
- Amantadine - SE: ataxia, slurred speech, confusion, livedo reticularis
- COMT inhibitors can be added to levodopa in advanced PD e.g. entacapone
- Antimuscarinic e.g procyclidne - good for drug induced parkinsonism (helps tremor + reigidity)
Give features of the following muscular dystrophies:
- Duchenne muscular dystrophy
- Becker muscular dystrophy
- Myotonic Dystrophy
Duchenne Muscular Dystrophy
- X-linked recessive. No functional dystrophin. CK v high.
- More severe than becker
- –> progressive prox muscle weakness from 5yo (-> waddling gait), calf pseudohypertrophy, gower’s sign (uses arms to stand), intellectual impairment
- Reduced life expectance (late 20s)
- Mx: physio, CPAP, araluren
Becker Muscular Dystrophy
- Still some functional dystrophin so less severe. Onset >10yo w/ slower onset
- Intellecular impairment much less common
- Life expectancy = middle or old age
Myotonic Dystrophy
- Autosomal dominant. Affects: skeletal, cardiac + smooth
- Most common muscular dystrophy in adults, onset 20-30y
- Multi system (not just muscles)
- Facial + jaw weakness, temple hollowing
- Frontal balding
- CVS -condution problems
- GI _ raised LFTs, gallstones, dysphagia
- Eyes - ptosis, cataracts, blepheraritis
How do you calcuate GCS?
Eyes (4)
4 - spontaneous opening
3 - open to voice
2- open to pain
1 - no opening
Voice(5)
5 - alert + oriented
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1- no speech
Motor (6)
6- follows commands
5- localises pain
4- withdrawal from pain
3- flexion to pain
2- extension to pain
1- no movement
Where is the damage in the following visual field defects?
- Homonymous Hemianopia
- Homonymous Quadrantanopia
- Bitemporal Hemianopia
Homonymous hemianopia
- without macular sparing: lesion of optic tract or both radiations (e.g. TACI or PACI stroke)
- with macular sparing = posterior stroke affecting occipital cortex
Homonymous quadrantanopia
- Superior: lesion in temporal/inferior optic radiation (meyer’s loop)
- Inferior: lesion in superior/parietal optic radiation
Bitemporal hemianopia
- Optic chiasm
- Superior bitemporal quadrantanopia due to inferior compression e.g. pituitary tumour
- Lower bitemporal quadrantanopia due to superior compression e.g. craniopharyngioma
