Core

Question 1

Stroke - sudden onset neuro signs:

1. What are the main causes of haemorrhage (4) and ischaemic (2) stroke?
2. In which ethnicities is stroke more common?
3. What is a watershed stroke? Where do they normally occur?
4. What features are required for TACS, PACS, POCS and LACS?
5. What is locked-in syndrome? Which artery is likely occluded?
6. A stroke in which artery can cause lateral medullary syndrome? What are the signs?(4)
7. What are the common vessels ruptured in haemorrhagic stroke?(3)

Answer 1

1. Haemorrhagic = HTN, amyloidosis, anticoagulation, ruptured aneurysm
   Ischaemic = atheroma and emboli
2. Black and Asian
3. Ischaemic stroke due to drop in SBP >40mmhg - can be caused by sepsis. In the area with shared blood supply from MCA and ACA.
4. TACS = contralateral hemiplegia/hemiparesis in 2 or more of UL/LL/Face, contralateral homonymous hemianopia, evidence of higher cortical dysfunction (Visio-spatial loss, dysphasia)
   PACS = 2/3 of TACS
   POCS = isolated contralateral hemianopia, cerebellar or brainstem syndrome
   LACS = pure sensory or motor, sensory-motor or ataxic hemiparesis
5. Vertebral pons infarct - basilar artery
6. In the posterior inferior cerebellar artery - Vertigo, trunk ataxia, N+V and nystagmus
7. Intraparenchymal, subarachnoid and intracerebral vessel

Question 2

Stroke Managment:

1. What are the immediate steps in stroke management? (5)
2. What is the drug Rx for secondary prevention for stroke? (2)
3. What are the two main rehabilitation factors which need to be prevented?
4. What is a CHA2DS2-VASc score? What do the scores mean?
5. What is a HASBLED score?
6. What is the drug Mx for someone with ischaemic stroke and AF?

Answer 2

1. Resuscitate and call stroke ward
2. Monitor BP and BM
3. Imaging - urgent CT to rule out haemorrhagic
4. Medical: Thrombolysis if CT head not suggestive of haemorrhage and <4.5 hours = alteplase.
   Aspirin 300mg once haemorrhage is excluded
5. Surgical: neurosurgery opinion if there is haemorrhage
6. Clopidogrel 75mg/day for life or Warfarin if cardioembolic stroke or AF.
7. DVT and pressure sores
8. Assess the risk of stroke in a patient with AF to see if anticoagulation is necessary
   0 = no anticoagulation necessary
   1 = consider anticoagulation if male
   2+ = offer anticoagulation
9. The risk of haemorrhage with anticoagulation
10. Aspirin daily, start long term anticoagulation after 2 weeks

Question 3

Meningitis:

1. What is the main causative organism in 6-60y/o?
2. What is the main causative organism in >60s?
3. What is the main causative organism in <5y/o?
4. What is the likely causative organism in a HIV patient?
5. What are some viral causes of meningitis? (3)
6. What Abx are given for bacterial meningitis >55 and <55?
7. What prophylactic Abx should be given to friends and family?
8. What should be given in addition to Abx in treating bacterial meningitis?
9. What are the CIs to LP? (4)
10. What is the most common complication of meningitis?
11. What drug is given for viral meningitis?

Answer 3

1. Neisseria meningitidis
2. Strep pneumoniae
3. Haemophilus influenzae B
4. TB
5. HSV, VSV, enteroviruses
6. > 55 = ceftriaxone + amox + dex
   <55 = ceftriaxone + dex
7. Ciprofloxacin
8. Dexamethasone
9. Thrombocytopenia, raised ICP, unstable, focal neuro signs
10. Sensory-hearing loss
11. Acyclovir

Question 4

Subdural and Extradural Haematoma:

1. Who is a greatest risk for these bleeds? (2)
2. What is the risk of an untreated subdural? (2)
3. What does and acute and chronic subdural haematoma look like on CT? What is important to check for?
4. What is the likely ruptured vessel in chronic subdural haematoma?
5. How do chronic subdurals present? (3)
6. What are the 1st and 2nd lines of treatment for subdural?
7. Which artery is typically damaged in extradural haemorrhage?
8. How do extradural’s present? (3)
9. What do extradural’s look like on CT? How are they managed?
10. What might you see O/E with an extradural haemorrhage?

Answer 4

1. Those on anticoagulation and the elderly
2. Tentorial herniation and coning
3. Acute = hyper-dense crescentic collection
   Chronic = hypo-dense crescentic collection

Ask for ‘bone windows’ setting on CT to assess for skull#
4. Bridging veins between cortex and venous sinuses in subdural space
5. Week to month progressive confusion, reduced consciousness or neurological deficit
6. 1st = Burr hole craniostomy irrigation and evacuation
2nd = craniotomy (organised clot)
7. Middle meningeal artery
8. Fluctuating consciousness, raised ICP, brainstem compression
9. Biconvex and hyper-dense - surgical removal
10. Fixed dilated pupil due to CNIII parasympathetic fibre compression

Question 5

What signs would be seen in septicaemic pt. vs meningitic?

Answer 5

Septicaemic = increased CRT, hypotension, cold hands + feet 
Meningitic = neck stiffness + photophobia

Question 6

Seizures/Epilepsy:

1. What are the most common causes of seizure? (4)
2. What are the congenital causes of seizure? (3)
3. What can cause a provoked/non-epileptic seizure? (4)
4. What is the difference between simple and complex focal seizure?
5. Describe the Jacksonian march, when is it seen?
6. Where do most focal seizures arise form?
7. What are generalised seizures? What are the main types? (6)
8. What are the signs localising seizure activity to each lobe?
9. What are the driving restrictions surrounding epilepsy?
10. What are the indications for MRI in suspected epilepsy? (3)
11. Which Ix is used to support a diagnosis of epilepsy?
12. What is the 1st and 2nd Rx for focal seizures?
13. What is the Rx for: tonic-clonic, absence and atonic/myoclonic seizures?

Answer 6

1. Idiopathic, congenital, CVA, drugs
2. Neurofibromatosis, Tuberous Sclerosis, perinatal anoxia
3. Metabolic= glucose, Na+, Ca2+ and urea
   Infection = meningitis + encephalitis
   Withdrawal = alcohol, benzodiazepines and opiates
   Raised ICP
4. Simple focal = seizure activity (any change in motor, sensory or autonomic function) arising from one hemisphere of the brain with no LOC

Complex focal = same as simple but LOC or impaired awareness

5. Seizure activity starting with distal and small muscle twitching which ascends proximally to larger muscles - simple focal seizures
6. Temporal lobe
7. Seizure activity arising from both hemispheres.
   Tonic-clonic - LOC, post-ictal confusion, tongue biting, incontinence
   Myoclonic - sudden muscle twitching
   Atonic - sudden loss of muscle tone with no LOC
   Febrile - children following CNS infection or electrolyte imbalance
   Absence - childhood with abrupt onset <10s
   West-syndrome/infantile spasms (cluster of head nodding and arm jerks)
8. Frontal = motor features
   Temporal = automatisms, deja vu, emotion, taste/smells
   Parietal = paraesthesia
   Occipital = visual changes
9. Advise not to drive after any seizure, if a diagnosis of epilepsy has been made then can’t drive until seizure free for >1 year
10. Adult onset, any evidence of focal onset or seizures despite 1st line Rx
11. EEG - cannot exclude nor prove only supports clinical suspicion
12. 1st = lamotrigine or carbamazepine
    2nd = oxycarbazepine
13. Tonic-clonic = lamotrigine (G) or valproate (B)
    Absence = ethosuxamide (G) or valproate (B)
    Atonic/myoclonic = leretiracetam (G) or valproate (B)

Question 7

Dementia:

1. What are the two distinctive hallmarks of AD?
2. Which three main areas with those with AD find the greatest difficulty in?
3. What would make you consider a diagnosis of AD as the cause of dementia?
4. Which will MRI of a patient with AD show?
5. What is the drug Mx for AD?
6. What factors may make you consider a diagnosis of vascular dementia? (Onset, RFs and rate of deterioration)
7. What is the likely cause of vascular dementia? What might be seen on MRI? (2)
8. What may make you consider a diagnosis of Lewy body dementia in terms of symptoms? (3)
9. How do you manage Lewy body dementia?
10. What may point to a diagnosis of fronto-temporal dementia in terms of symptoms? (3)
11. Before considering a diagnosis of dementia, what are some ameliorable causes of the symptoms? (5)

Answer 7

1. Senile plaques and neurofibrillary tangles
2. Visio-spatial, memory and executive planning
3. Enduring, progressive cognitive decline
4. Medial temporal lobe atrophy
5. Anti-cholinesterase
6. Onset = sudden
   RFs = vascular RFs
   Rate = step-wise
7. CVA resulting in multiple infarcts - multiple infarcts or small vessel disease
8. Fluctuating cognitive decline, visual hallucinations and Parkinsonism
9. Anti-cholinesterase
10. Disinhibition, personality changes, progressive aphasia
11. Infection, chronic subdural, neoplasia, B12 and folate, normal pressure hydrocephalus

Question 8

MS:

1. Which gene is associated with MS?
2. What is the common presentation of MS? (PEAS)
3. Describe the main subtypes of MS? (3)
4. What are Lhermitte’s and Uhthoff’s phenomena? When are they seen?
5. Which Ix is diagnostic?What might you find on LP with MS?
6. Which criteria may aid MS diagnosis?
7. What drug do you give to manage acute attacks in MS?
8. Which drugs do you give to prevent relapses in MS? (2)
9. What is the drug Mx for the symptoms of MS? (Fatigue, depression, pain, spasticity, urgency/frequency and tremor)

Answer 8

1. HLA-DRB1
2. Paraesthesia, eye (optic neuritis), Ataxia, Spastic paraparesis
3. • Relapsing-remitting (85%) = acute attacks lasting 1-2 months followed by periods of remission
   • Primary progressive (10%) = progressive deterioration from onset which is more common in older people
   • Secondary progressive = relapsing-remitting patients with neuro signs developed between relapses (mainly gait and bladder disorders are seen). 65% of relapsing-remitting patients develop secondary progressive disease within 15 years.
4. Lhermitte’s = flexion of the neck = tingling down neck and back (MS + cervical spondylosis)
   Uhthoff’s = worsening of symptoms in heat (MS)
5. MRI
   IgG oligoclonal bands which are absent in serum, shows CNS inflammation
6. McDonald Criteria
7. Methylprednisolone for 5 days
8. Biologics + DMARDs

9. Fatigue = modafinil 
Depression = citalopram 
Pain = amitriptylline 
Spasticity = Baclofen 
Urgency/frequency = oxybutinin 
Tremor = clonazepam

Question 9

Cerebral Abscess:

1. What are the main causes? (3)
2. What are the main causative bacterial (3) and fungal organisms (3)?
3. In which type of patients is fungal cerebral abscess more likely to be in? (3)
4. What are some of the signs/symptoms of cerebral abscesses? (4)
5. Which Ix confirms the diagnosis - what is the hallmark feature?
6. What is the medical (2) and surgical management?

Answer 9

1. Middle ear or sinus infection, trauma or surgery to scalp, emboli from endocarditis (rare)
2. S aureus, listeria, streptococcus
   Aspergillus, candida, cryptococcus
3. Those with broad spectrum Abx, immunosuppressed and steroids
4. Fever, signs of raised ICP, altered mental state and focal neurology to the site of the abscess
5. Contrast CT - ring enhanced lesion
6. Medical = IV ceftriaxone + metronidazole
   Surgical = craniotomy to debride the abscess

Question 10

CN Palsies:

1. Down and out eye, ptosis + miosis is associated with which CN? What are the main causes? (3)
2. What is trigeminal neuralgia? What are the causes?(2) How does it present?
3. What are the red flag signs of trigeminal neuralgia? (3) How is it managed normally? When is urgent referral required?
4. Which CN palsy may present with internucelar ophathalmoplegia and conjugate lateral gaze disorder with diplopia?

Answer 10

1. Third nerve palsy - DM, vasculitis + PCA aneurysms
2. Pain syndrome of the trigeminal nerve, idiopathic and compression of trigeminal nerve roots may occur.

Presents as sudden onset ‘stabbing’ pains in one or more of the divisions of the trigeminal nerve - evoked by light touch and last seconds to minutes

3. Red flags = <40 y/o, hearing changes, pain only in ophthalmic division - requires urgent referral

Otherwise Rx via carbamaezpine - failure to respond = urgent referral

4. CNXI - there is inability for the affected eye to abduct

Question 11

MND:

1. What are the main diseases regarded under MND? (4)
2. What might point to a diagnosis of MND? What signs are seen O/E?
3. How would you distinguish MS and MND? (2)
4. Which medication is given to control drooling in MND? (2)
5. How do you reduce spasticity in MND?
6. Which drug class may delay mortality? Which blood test can it affect?
7. Which muscles are spared in MND?

Answer 11

1. ALS (amyotrophic lateral sclerosis), progressive muscular atrophy, bulbar palsy and primary lateral sclerosis
2. Age 40+ with spastic stumbling gait and foot drop, weak grip and weak shoulder abduction - UMN +LMN signs with absence of sensory or cerebellar signs
3. No sensory change or sphincter disturbance in MND
4. Amitriptyline or propantheline
5. Baclofen
6. Anti-glutaminergic drugs (riluzole) - can derange LFTs
7. Extra-ocular

Question 12

Bulbar palsy and pseudobulbar palsy:

1. What is bulbar palsy? Where are the lesions usually?
2. What are the signs of bulbar palsy? (3)
3. What are the causes of bulbar palsy? (4)
4. How is pseudobulbar palsy different to bulbar palsy? Where are the lesions usually?
5. What are the signs of pseudobulbar palsy? (3)
6. What are the causes of pseudobulbar palsy? (4)

Answer 12

1. Diseases of nuclei CN IX-XII in the medulla
2. LMN lesions of tongue (flaccid and fasciculating), speech is quiet and nasal, dysphagia
3. MND, GBS, MG, central pontine myelinosis
4. Similar symptoms but due to UMN bilateral lesions above the mid pons.
5. Spastic tongue, slow tongue movements and brisk jaw jerk
6. Stroke, MS, MND, Central pontine myelinosis

Question 13

CNS tumours:

1. What are the most common types of brain tumour? (2)
2. How are they diagnosed?
3. Which drug is given to manage cerebral oedema?
4. Which tumours most commonly metastasise to the brain? (4)
5. Why can’t gliomas be managed surgically?

Answer 13

1. Glioma or metastatic
2. MRI
3. Dexamethasone
4. Lung (most common), breast, bowel, melanoma
5. Have a propensity to invade the brain tissue quickly

Question 14

How do you differentiate between a syncopal and seizure LOC?

Answer 14

Syncope seizures have rapid recovery and <2min post-ictal period. Seizure post octal periods last at least 15mins.

Question 15

GBS:

1. What is the pathophysiology?
2. What is the classic causative organism?
3. What is the pattern of weakness?
4. What reflex change may be seen?
5. What Ix can confirm GBS? (2)
6. What is the management?
7. What are some complications to be aware of?

Answer 15

1. Immune-mediated demeylination of the peripheral nervous system triggered by infection
2. Campylobacter jejuni
3. Progressive ascending weakness (from legs to arms - proximal muscles to distal)

Sensory changes may also be present

4. Reduced or absent
5. LP (raised protein) and nerve conduction studies

Isolated raised protein on LP is highly suggestive of GBS

6. IV immunoglobulins
7. Respiratory depression, bulbar symptoms, autonomic dysfunction

Question 16

Migraine:

1. What are the features of a migraine headache? (4)
2. What is the difference between a classical migraine and common migraine?
3. What is the drug management for an acute migraine attack? (2)
4. What is the drug management for migraine prophylaxis? (2) When should it be offered? What is second line for migraine prophylaxis?
5. What drug should be offered for prophylaxis of menstrual triggered migraines? (2)

Answer 16

1. • Unilateral + throbbing 4-72 hours
   • Phono/photophobia
   • Prodome (50%) - hours or days preceding migraine
   • Aura (20%) - preceding migraine by minutes
2. Classical = with aura
   Common = no aura
3. 1st = oral triptan + NSAID/paracetamol
4. Propranolol (better for women of child bearing age) or topiramate (if asthmatic)- offered if there are 2+ attacks per month

2nd line = accupuncture

5. Triptans or NSAIDs around the time of menstruation

Question 17

Myasthenia Gravis:

1. What is the pathophysiology?
2. What are the main auto-antibodies in MG? (3)
3. How does it present? Which muscles are commonly affected (4) and what is the pattern of weakness?
4. Which drugs can worsen the weakness? (5)
5. Which cancer is associated with MG?
6. What Ix can confirm MG? (2)
7. What is the drug treatment for symptomatic control and for reducing relapses?
8. What is the surgical management for MG? When is it indicated?
9. What is a myasthenic crisis? What are the triggers? How is it managed? (2)

Answer 17

1. Auto-immune mediated production ACh receptor antibodies which bind to nicotinic ACh receptors on post-synaptic neurones preventing ACh from binding - results in less effective muscle stimulation.
2. 85% = ACh receptor antibodies
   15% = MuSK (muscle specific kinase) and LRP4 (low density lipoprotein receptor-related protein 4) antibodies.
3. Increasing muscle fatigue. Commonly affects extra-ocular muscles (bilateral ptosis + diplopia), bulbar, facial and neck muscles.
   Weakness which increases the more the muscles are used - symptoms usually worse at the end of the day
4. B-blockers, gentamycin, opiates, tetracyclines, phenytoin
5. Thyoma
6. Auto-antibodies for AChr, MuSK and LRP4 + endrophonium test (endrophonium blocks cholinesterase enzymes so temporary relief of weakness)
7. Symptomatic control = Pyridostigmine (anticholinesterase)
   Relapses = prednisolone (suppresses antibody production)
8. Thymectomy - <50y/o not responding to anticholinesterase
9. Acute worsening of symptoms causing weakness of respiratory muscles - triggered by respiratory tract infection and medications.

Mx = BiPaP and IV immunoglobulins or plasma exchange

Question 18

Status epilepticus:

1. What are the management steps? (5)
2. What can be given to an alcoholic patient in status? (2)
3. What must be monitored when starting phenytoin?

Answer 18

1. -ABCDE: 15L high flow O2
   NB: Check blood glucose and hypoxia before commencing treatment!!! (Very easily correctable)

• IV access and IV lorazepam (stops seizure - repeat if no response in 10mins)
• If no response to double lorazepam or 25mins of status then start IV phenytoin (can cause long QT so ECG required)
• If no response within 45mins then consider GA

2. 200mg diazepam and thiamine
3. Cardiac monitoring - can be pro-arrhythmogenic

Question 19

Bell’s Palsy:

1. What is the cause?
2. What are the features? (2)
3. In which age group is most common in and who is at greatest risk? (2)
4. How is the diagnosis made?
5. How is managed? (2)

Answer 19

1. Usually idiopathic but associated with HSV
2. Sudden onset with complete unilateral facial weakness or paralysis with dry eyes due to inability to close eyelid - LMN lesion
3. 20-40 y/o + pregnant and DM
4. Diagnosis of exclusion
5. Prednisolone within 72hrs and protect the eye

Question 20

Cranial Nerves:

1. What are the features of CN III - CN XII palsies?

Answer 20

III = down and out eye, ptosis and dilated fixed pupil 
IV = defective downward gaze (vertical diplopia) - contralateral 
V= trigeminal neuralgia, loss of facial sensation and corneal reflex 
VI = defective abduction (horizontal diplopia) - ipsilateral 
VII = Bell’s palsy + loss of taste 
VIII = hearing/balance problems 
IX = loss of gag reflex 
X = uvula deviation away from lesion 
XI = weakness turning head 
XII = tongue deviates towards lesion

Question 21

Encephalitis:

1. When would you suspect encephalitis?
2. How do you differentiate between encephalitis and encephalopathy?
3. What are the main causative organisms?
4. What Ix would you do? (2)
5. What drug must you give on admission?
6. Which lobes are commonly affected? (2)

Answer 21

1. If there is reduced consciousness, confusion, seizure or focal neurology following signs of infection e.g. temperature, rash and meningism
2. Encephalopathy won’t have an infectious ‘pro-drome’
3. Viral (more common) - esp. HSV-1 (95% of cases in adults)
   Bacterial = meningitis, TB, malaria
4. Contrast enhanced CT (HSV = bilateral temporal lobe involvement) or MRI if allergic to contrast
   LP - send for viral PCR (moderate protein and lymphocytes)
5. Acyclovir within 30mins
6. Medial temporal and inferior frontal

Question 22

Normal Pressure Hydrocephalus:

1. What is the triad of presentation?
2. What is the duration for the development of symptoms?
3. What will be seen on MRI? (3)
4. How is it managed? What are the complications of this management?(3)

Answer 22

1. Urinary incontinence, dementia and gait abnormality
2. A few months
3. Hydrocephalus with fourth ventricle hypertrophy with an absence of sulcal atrophy
4. Ventriculoperitoneal shunting - seizures, infection, intracerebral haemorrhages

Question 23

Subarachnoid Haemorrhage:

1. What are the two most common causes of SAH?
2. What are the common sites for berry aneurysms? (3)
3. Which conditions are associated with increased risk of SAH? (3)
4. What is the definitive Ix for SAH?
5. If SAH is strongly suspected but CT is -ve for haemorrhage, what is the next line Ix? What would be seen?
6. What immediate action needs to be taken with suspected SAH?
7. How should you initially manage a patient with SAH? (2)
8. What is the surgical Mx for SAH?
9. What are the main complications? (4)

Answer 23

1. Rupture of saccular aneurysms (80%) and AVM (15%)
2. Bifurcation of MCA and junction between:
   - Anterior communicating artery and ACA
   - Posterior communicating artery and PCA
3. APCKD, CoA, Ehlers Danlos
4. CT Head - hyper-dense collection around the circle of willis (only with ruptured berry which is most common)
5. LP - xanthochromia (yellow CSF due to bilirubin breakdown from blood in CSF)
6. Call neurosurgery
7. Maintain SBP >160mmHg and Nimodipine 60mg/4h (CCB - reduces vasospasm and consequent morbidity from ischaemia)
8. CT angio then endovascular coiling

9. 
Re-bleeding 
Cerebral ischaemia 
Hydrocephalus 
Hyponatraemia

Question 24

TIA:

1. What are the main causes of TIA? (3)
2. What causes amaurosis fugax?
3. What does the ABCD2 score predict? What does a score of 4 and 6 mean?
4. What four things should be done when someone is admitted with suspected TIA?
5. What % of carotid artery stenosis are endartectomies useful?
6. What is the alternative to endartectomy? What is the main complication?
7. How do you differentiate an ischaemic stroke and TIA?
8. Which metabolic change can present very similarly to TIA?
9. When is a CT head indicated with TIA?

Answer 24

1. Atheroembolism from carotids, cardioembolism, hyperviscosity
2. Emboli passing through retinal artery
3. Risk of stroke following TIA, 4 = specialist assessment within 24hours, 6= 35% chance of stroke in 1 week
4. Anti-platelet therapy, CVS Rf assessment, ABCD2 score, specialist referral
5. 70%+, 50-70% may be useful
6. Endovascular stenting - in-stent resentosis
7. There is no infarct with TIA on CT (if found then it is a stroke)
8. Hypoglycaemia
9. If they’re on any form of anticoagulant

Question 25

Parkinson’s: 1. What are the four cardinal features? 2. What is the pathophysiology of PD? (2) 3. What are the main complications of PD? (5) 4. What are the Parkinson’s + syndromes? (4) How do you differentiate them from PD? 5. Which infections could lead to Parkinsonism? (2) 6. Which genetic disorder has a pre-disposition to Parkinsonism? 7. Which drugs can cause Parkinsonism? (2) 8. Which drug is given to treat early motor symptoms of PD? What should be subsequently given if there is a reemergence of motor symptoms despite Rx? 9. Which drugs are given in early PD if there is no motor impact of PD? (2) 10. What is the 1st line Rx for an essential tremor? 11. Which drugs should be avoided in PD and Parkinson’s +? (4) 12. Which anti-emetic can be prescribed in PD?

Answer 25

1. Bradykinesia, rigidity, resting tremor, postural instability 2. Destruction of dopaminergic neurones in substantial nigra and B-amyloid plaques and neurofibrillary tangles in SN 3. Sleep disorder (90%), depression, postural hypotension, psychosis, constipation 4. MSA - autonomic dysfunction Progressive supranuclear palsy - early falls, gaze palsy Corticobasilar degeneration Lewy body dementia - early cognitive decline and hallucinations 5. HIV and syphilis 6. Wilson’s disease 7. Anti-psychotics and metclopramide 8. 1st = L-dopa 2nd = L-dopa + dopamine agonist/COMTi/MAO-Bi 9. Dopamine agonists and MAO-Bi 10. Propranolol 11. Cyclizine/prochlorperazine (anti-histamines), haloperidol, metclopramide - can block D2 receptors which worsen PD symptoms 12. Domperidone

Question 26

1. Which drugs are associated with Steven-Johnson syndrome? (2) 2. What is the MOA of anti-epileptic drugs? 3. What are the main SEs of carbamazepine? (6) 4. What are the acute SEs (5)of phenytoin? What are the chronic SEs of phenytoin? 5. Which anti-epileptics are CI with sinus bradycardia and bone marrow suppression? (2) 6. Who must phenytoin not be given to? What can it cause? (2) 7. What is the MOA of sodium valproate? What are the main SEs? (7) 8. Which drugs are associated with the P450 enzyme? (3) 9. What is the MOA of triptans? What is the main SE? What is the CI? (2) 10. What are the main SEs of L-dopa? (4) 11. If L-dopa can’t be taken orally, what is given instead? 12. What are the main cholinesterase inhibitors? 13. What is SJ syndrome? How is it managed?

Answer 26

1. Carbamazepine and lamotrigine 2. Block voltage gated Na+ channels to increase the AP refractory period. 3. Dizziness and ataxia, lethargy and drowsiness, headache and diplopia and SJ syndrome 4. Acute: dizziness and ataxia, diplopia and nystagmus, confusion Chronic: gingival hyperplasia, hirsutism, drowsiness 5. Phenytoin and carbamazepine 6. Pregnant women - upper cleft palate and congenital heart disease 7. Increases GABA activity - alopecia, weight gain, N+V, tremor, hepatotoxicity, pancreatitis, thrombocytopenia 8. Carbamazepine + phenytoin = P450 inducers Valproate = inhibitor 9. 5-HTP agonists, tingling or flushing with heaviness or pressure on throat/chest. CI = history of or RFs for ischaemic heart disease or cerebrovascular disease 10. Rarer but: dyskinesia, on-off effect, N+V, psychosis 11. Dopamine agonist patch. 12. Donepezil, rivastigmine, galantamine 13. Severe systemic reaction affecting the skin and mucosa - maculopapular with ‘target lesions’ with systemic symptoms e.g. fever and arthralgia - admission for supportive Mx

Question 27

Visual Field Defects: 1. What would cause complete vision loss in one eye? 2. What causes a homonymous superior and inferior quadrantantopia? PITS 3. What are the causes of a bitemporal hemianopia? (3) 4. What are the causes of a homonymous hemianopia? (3)

Answer 27

1. Optic nerve lesion 2. Superior = temporal lobe Inferior = parietal lobe 3. Lesion of optic chiasm Upper quadrant defect > lower quadrant defect = inferior chiasm compression = pituitary tumour Lower quadrant defect > upper quadrant defect = superior chiasm compression = craniopharyngioma 4. Lesion of occipital cortex (macula sparing), lesion of optic radiation or lesion of optic tract

Question 28

Radiculopathies: ``` What are the a) Nerve roots b) Motor innervation c) Sensory innervation d) Clinical presentation of damage For the radial, ulnar, median nerves? ```

Answer 28

1. Radial Nerve root = C5-T1 Motor innervation via main branch = triceps, brachioradialis, anconeus and extensor carpi radialis Motor innervation via interosseus branch = supinator and extensor muscles of hand Sensory innervation = dorsal lateral 3.5 digits (- the finger tips) Clinical presentation 1. wrist drop and sensory loss of dorsal aspect of 1st and 2nd metacarpals 2. Axillary damage = as above + tricep paralysis 2. Ulnar Nerve root = C8 and T1 Motor innervation = aDductor pollicis, hypothenar muscles, flexor carpi ulnaris, interossei and medial two lumbricals Sensory innervation = Medial 1.5 fingers (dorsal and palmar) Clinical presentation depends on where damage is: 1. At wrist = ‘claw hand’, sensory loss and wasting of intrinsic hand muscles 2. At elbow = as above but radial wrist deviation 3. Median Nerve root = C5-T1 Motor innervation = mainly flexors Sensory innervation = same 2.5 fingers as ulnar but palmar aspect and tips of fingers dorsally Clinical presentation: 1. At wrist = carpal tunnel 2. At elbow = carpal tunnel + unable to pronate, flex wrist an ulnar deviation Think anterior interosseus (branch of median) if unable to pronate and weak flexion of thumb and index