Neuro Flashcards

1
Q

Which drugs can cause Parkinsonism?

A

Anti psychotics - clozapine, quietapine, haloperidol, risperidone
Anti emetics - Metoclopramide and prochlorperazine
Methyldopa (BP)
Calcium channel blockers - cinnarizine and flunarizine
Amiodarone
Sodium valproate
Lithium

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2
Q

What is juvenile Parkinson’s?

A

Diagnosis under age 20

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3
Q

What is early onset Parkinson’s?

A

Diagnosis under age 40

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4
Q

What are the Parkinson’s plus syndromes?

A

Multiple system atrophy
Progressive supranuclear palsy
Corticobasal degeneration

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5
Q

What are signs and symptoms of multiple system atrophy?

A

Autonomic dysfunction
Parkinsonism
Ataxia

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6
Q

What is a DaTSCAN?

A

Dopamine transporter SPECT scan used in diagnosis of PD

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7
Q

If a GP suspects early stages of PD, how soon should the pt see a specialist (neurologist or geriatrician)?

A

Within 6 weeks

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8
Q

If a GP suspects late stages of PD, how soon should the pt see a specialist (neurologist or geriatrician)?

A

Within 2 weeks

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9
Q

How is a diagnosis of Parkinson’s made?

A

Usually clinical diagnosis
Likely PD if at least 2 of: resting tremor, bradykinesia, rigidity
If symptoms improved by levodopa - more likely
DaTSCAN can be used to aid diagnosis

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10
Q

What are the groups of causes of Parkinsonism?

A

Idiopathic
Drug induced
Cerebrovascular
Other progressive brain conditions - Parkinson’s plus

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11
Q

What development assessment tool is used for children?

A

SOGS II - birth to 5 years
Schedule of growing skills
Screening tool

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12
Q

What 9 areas are assessed in SOGS II?

A
Passive posture 
Active posture 
Locomotor 
Manipulative 
Visual
Hearing and language 
Speech and language 
Interactive social
Self care social
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13
Q

What factors contribute to idiopathic intracranial hypertension?

A

Pregnancy
Combined oral contraceptive therapy
Obesity
Oral tetracycline therapy

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14
Q

How do you treat idiopathic intracranial hypertension?

A

Weight reduction
Stopping the offending drug
More serious where sight is threatened - cerebrospinal fluid removal of shunting may be required

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15
Q

What is recommended for carotid artery stenoses greater than 70% diameter?

A

Carotid endarterectomy

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16
Q

What are complications of subarachnoid haemorrhage?

A

Recurrent SAH
Vasospasm
Stroke
Hydrocephalus

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17
Q

What are features of subarachnoid haemorrhage?

A
Acute onset severe headache
Meningeal irritation
Low grade fever
Localising neuro signs 
Neurogenic pulmonary oedema
ST elevation on ECG
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18
Q

What problems does maternal narcotic addiction cause in a neonate?

A

Neonatal abstinence syndrome: tremors, irritability, sleep problems, high pitched crying, hypertonia, hyperreflexia, seizures, mottled skin, fever, slow weight gain
Symptoms usually 1 to 3 days after birth

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19
Q

What might convulsions occurring in first 24 hours of life signify?

A

Placental insufficiency

Cerebral palsy

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20
Q

What are some causes of horners syndrome?

A
Pancoast tumour
Cervical rib
Goitre
Syringomyelia 
Lateral medullary syndrome - brainstem stroke
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21
Q

Which is the best choice of antiepileptic drug for generalised epilepsy in women of child bearing age? What supplement should be given alongside during pregnancy? And what screening is required?

A

Lamotrigine
High dose folate supplements
Vitamin K given to mother prior to delivery
Alpha fetoprotein and second trimester USS screening

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22
Q

Why would phenytoin and valproate not be sensible choices for antiepileptic treatment in a woman of child bearing age?

A

Teratogenic effects

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23
Q

What is Patterson Kelly Brown syndrome?

A

Plummer Vinson syndrome
Triad of microcytic hypochromic anaemia
Atrophic glossitis
Oesophageal webs/stricture

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24
Q

What is Webers syndrome?

A

Infarction of the midbrain
Contralateral hemiplegia
Ipsilateral oculomotor nerve palsy and diplopia

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25
Q

What is Charcot Marie tooth disease?

A

Autosomal dominant inherited condition

Wasting of lower limbs and small muscles of hands

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26
Q

What is diabetic amyotrophy?

A

Weakness, wasting and pain usually in quadriceps
Paraesthesia of the proximal lower limbs - thigh, hip, buttock
Symptoms begin on one side but usually spread to other
Vasculitic changes, microvascular insufficiency and ischaemia followed by axonal degeneration and demyelination

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27
Q

What is friedreichs ataxia? What are features of it?

A

Progressive ataxia, dysarthria, decreased proprioception, ascending muscle weakness, pes cavus, scoliosis, cardiomyopathy, arrhythmias, diabetes
Inheritance autosomal recessive, decreased synthesis of frataxin - mitochondrial protein
Onset before 20 years

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28
Q

What is von Hippel Lindau disease?

A

Mutation in tumour suppressor gene
Multiple tumours in CNS and viscera
Most commonly retinal, haemangioblastomas, renal cell carcinoma, phaeochromocytoma
May be diagnosed from FH and genetic testing

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29
Q

What causes should be considered for prolonged hiccup?

A

CNS disease - posterior fossa tumour, brain injury, encephalitis
Phrenic nerve or diaphragm irritation - tumour, pleurisy, pneumonia, intrathoracic adenopathy, pericarditis, GORD, oesophagitis

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30
Q

What are causes of dilated pupils?

A

Holmes adie pupil
Third nerve palsy
Drugs and poisons - atropine, CO, ethylene glycol

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31
Q

What are causes of small pupils?

A
Horners syndrome
Old age
Pontine haemorrhage
Argyll Robertson pupil
Drugs and poisons - opiates, organophosphates
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32
Q

What are features of neuroleptic malignant syndrome?

A
Fever
Rigidity
Altered mental status 
Autonomic dysfunction
Elevated creatine phosphokinase
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33
Q

Concomitant use of which drugs may increase the risk of neuroleptic malignant syndrome?

A

Lithium or Anticholinergics alongside antipsychotic drugs

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34
Q

What is the treatment for neuroleptic malignant syndrome?

A

Withdrawal of the offending drug
Reduction of body temperature with antipyretics
Bromocriptine and amantadine - dopaminergic drugs
Dantrolene sodium - muscle relaxant

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35
Q

You are referred to a 40 year old woman in a psych ward who has a long history of schizophrenia resulting in multiple hallucinations in the past. She gives a several week history of feeling generally unwell associated with increasing stiffness affecting the jaws and arms. Over the last few years she has been on haloperidol with good symptom control. Her temp was 38.5 and BP 175/85. What does she have and what is the most important investigation to be performed?

A

Neuroleptic malignant syndrome

Creatine phosphokinase

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36
Q

What causes meralgia paraesthetica?

A

Damage to the lateral cutaneous nerve of the thigh

Usually due to entrapment at the lateral inguinal ligament, trauma, ischaemia or a retroperitoneal lesion

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37
Q

What is alports syndrome?

A

Inherited condition of sensorineural deafness and renal dysfunction - glomerulonephritis
Defect in type IV collagen

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38
Q

What are features of an acoustic neuroma?

A
Hearing loss - sensorineural 
Unilateral tinnitus 
Vertigo 
Pressure in ear
Facial numbness and tingling
Loss of corneal reflex
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39
Q

What is the alternative name for an acoustic neuroma? What cells does it affect?

A

Vestibular schwannoma

Schwann cells

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40
Q

What is the triad of features of wernickes encephalopathy?

A

Acute mental confusion
Ataxia
Opthalmoplegia

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41
Q

What are the oculomotor findings in wernickes encephalopathy?

A

Weakness of abduction
Gaze evoked nystagmus
Internuclear opthalmoplegia
Vertical nystagmus in primary position

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42
Q

What are some causes of wernickes encephalopathy?

A
Chronic alcohol abuse
Dialysis patients
Advanced malignancy
AIDS
Malnutrition
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43
Q

What is the urgent treatment for wernickes encephalopathy?

A

100mg fresh thiamine IV followed by 50-100mg daily

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44
Q

What can cause cerebral abscess?

A

Untreated or partially treated meningitis
TB
Pyogenic ear infections
Facial/orbital cellulitis

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45
Q

What is treatment for cerebral abscess?

A

Surgical drainage

Abx

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46
Q

What are signs and symptoms of cluster headache?

A
Severe unilateral pain in temple and periorbital region 
Attacks lasting a few moments to two hours 
Ipsilateral lacrimation
Nasal congestion
Conjunctival injection
Miosis
Ptosis
Lid oedema
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47
Q

What is the first choice of Abx in meningitis for different patient groups?

A

For infants 3m - adults 50 years, cefotaxime/ceftriaxone
If been outside UK recently or multiple Abx in last 3 months - add vancomycin
Under 3m and over 50, add amoxicillin to cover for listeria

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48
Q

What might be possible causes of a post op seizure out of the blue?

A
Severe hyponatraemic encephalopathy 
Hypoglycaemia 
Sepsis
Hypoxia 
Drug induced
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49
Q

What are sequelae of trigeminal nerve herpes zoster?

A

Trigeminal neuralgia
Corneal ulceration
Postherpetic neuralgia

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50
Q

Why might MS patients get urgency of urine?

A

Spastic paraparesis caused by demyelination in SC

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51
Q

Why might MS patients get episodes of visual disturbance?

A

Optic neuritis

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52
Q

A 63 year old hypertensive male presents with sudden onset vertigo, ataxia, diplopia and dysarthria. What is the problem?

A

Vertebrobasilar ischaemia

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53
Q

A 55 year old woman complains of recurrent severe stabbing pain in left cheek and jaw. The episodes last 5-10 secs and frequently occur during meals and showers. Examination of the cranial nerves is unremarkable. What is the drug of choice?

A

Carbamazepine

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54
Q

What medications should be used for prophylaxis of migraine?

A

Propranolol
Pizotifen
Topiramate

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55
Q

What medications can be used for acute attacks of migraine?

A

Sumatriptan

Ergotamine

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56
Q

A 53 year old administrator attends her GP complaining of pain in her R hand which is worse at night and relieved by hanging her arm off the side of the bed. What is the most likely diagnosis?

A

Carpal tunnel syndrome

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57
Q

Which nerve is implicated in carpal tunnel syndrome?

A

Median nerve

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58
Q

By what mechanism is the nerve affected in carpal tunnel syndrome?

A

Compression, traction, pinching, squeezing or irritation of the median nerve as it runs through the transverse carpal ligament

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59
Q

What structures form the carpal tunnel?

A

Scaphoid
Lunate
Triquetrium
Flexor retinaculum

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60
Q

Which tendons run through the carpal tunnel?

A

Flexor digitorum profundus x 4
Flexor digitorum superficialis x 4
Flexor pollicis longus

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61
Q

In which canal does the ulnar nerve run?

A

Guyons canal

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62
Q

What findings would you expect on examination of a person with carpal tunnel?

A

Scars from previous release surgery
Sensory loss lateral 3 and a half digits
Wasting and weakness of LOAF: first and second lumbricals, opponens pollicis, abductor pollicis brevis, flexor pollicis Brewis
Positive Phalens: tingling in median nerve distribution induced by full flexion of the wrists for 60 secs
Positive Tinels: tapping over median nerve at wrist generates tingling in nerves distribution

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63
Q

What conditions can predispose to carpal tunnel syndrome?

A
Diabetes
Hypothyroidism 
RA
Pregnancy 
Obesity 
Wrist fracture/trauma
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64
Q

What investigations can be done for carpal tunnel syndrome? What will they show?

A

EMG: electromyography shows focal slowing of conduction velocity in the median nerve across carpal tunnel, prolongation of the median distal motor latency, decreased amplitude of median sensory and/or motor nerves
USS wrist: space occupying lesion may be identified
MRI wrist: space occupying lesion may be identified, useful pre op

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65
Q

Describe EMG as you would to a patient

A

Electrodes attached to skin one which emits a signal, one which records
Electrical impulses given to nerve - feel like sharp tapping sensation on skin, bit unpleasant but doesn’t last long
Time it takes for muscle to contract is recorded - conduction velocity
If you take muscle relaxants or anti cholinergics, may need to stop them
Tell person doing test if you have a pacemaker or defibrillator
Avoid hand lotions/creams
Wear loose fitting clothing that can be rolled above elbow

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66
Q

What are management options for carpal tunnel syndrome?

A

Avoid activities which make symptoms worse
Treating underlying condition
Wrist splint: improvement in 4 weeks
Corticosteroid injection into wrist
Carpal tunnel release surgery when other treatments have failed

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67
Q

What are possible complications of carpal tunnel release surgery?

A
Infection
Persisting symptoms
Bleeding
Nerve injury
Scarring
Persistent wrist pain different from original 
Complex regional pain syndrome
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68
Q

What advice should be given after carpal tunnel release surgery?

A

Keep hand bandaged and raised for 2 days - sling
Gentle finger, shoulder and elbow exercise to prevent stiffness
Avoid using hand to do demanding activities until it is completely recovered which might take several weeks

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69
Q

A 35 year old man attends his GP complaining of severe pain in his L leg and numbness in his foot. His symptoms began suddenly 2 days ago when he bent down to pick up his child. He is otherwise fit and well. He also has back pain but less severe than his leg. What is the likely cause of his symptoms?

A

Sciatic nerve compression

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70
Q

What anatomical change causes sciatica?

A

Vertebral disc prolapse which causes compression on the sciatic nerve

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71
Q

What clinical test can you do to diagnose sciatica? What sign does this elicit?

A

Straight leg raise
Lasegues sign: pain in distribution of sciatic nerve reproduced with passive flexion of straight leg between 30 and 70 degrees

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72
Q

What is the management for sciatica?

A
Keeping active - exercise
Physio 
NSAIDs
Amitriptyline and duloxetine
Gabapentin and pregabablin
Corticosteroid injections
Muscle relaxants
Surgery: Open discectomy, microdiscectomy
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73
Q

A patient with a sciatic pain returns to the GP 3 days later with pain in both legs. What diagnosis needs to be urgently excluded and why? How do exclude it?

A

Cauda equina syndrome
Needs to be excluded quickly as can lead to paralysis, sensory changes, bladder bowel and sexual dysfunction
MRI

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74
Q

What questions do you need to ask to exclude cauda equina syndrome?

A
Unilateral or bilateral sciatica
Saddle and perineal anaesthesia 
Urinary retention/incontinence 
Faecal incontinence  
Lower extremity motor weakness and sensory deficits
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75
Q

What examination findings would you expect in cauda equina syndrome?

A
Back tenderness to palpation
Radicular sensory loss
Saddle anaesthesia 
Asymmetrical paraplegia
Loss of tendon reflexes
Poor anal sphincter tone
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76
Q

What is the management for cauda equina?

A

Urgent spinal decompression

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77
Q

A 54 year old dentist attends her GP complaining of cramps and weakness in her R hand which are starting to affect her work. On examination there is general wasting of the hand muscles with muscle fasciculation and a brisk wrist reflex. What is the most likely diagnosis? Why?

A

Motor neurone disease - mixed upper and lower motor neurone signs
ALS

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78
Q

Which nerve cells are affected in motor neurone disease?

A

Motor neurones in the ventral spinal cord

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79
Q

What is the likely prognosis for ALS?

A

Life expectancy 2 to 5 years

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80
Q

What symptoms do you see with progressive bulbar palsy?

A
Progressive dysphagia 
Dysphonia 
Dysarthria 
Wasted tongue with fasciculations
Drooling
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81
Q

What are symptoms of psuedobulbar palsy?

A
Slow and slurred speech
Dysphagia 
Spastic tongue
Brisk jaw jerk
Dysarthria
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82
Q

A fit and well 25 year old woman attends A and E complaining of weakness in her legs. 2 weeks ago she had an episode of food poisoning from which she made a full recovery. 5 days ago she started to get numbness in her toes which has spread to her feet ankles and shins. This morning she woke up and was unable to move her feet. She is very anxious. She has a mild low back ache. On examination tone is reduced in her lower limbs, there is sensory loss, weakness, reduced knee and absent ankle reflexes. What is the differential?

A
Guillain Barre syndrome 
Cauda equina and conus medullaris syndromes
Chronic inflammatory demyelinating polyradiculoneuropathy 
Myasthenia gravis 
Heavy metal toxicity 
Lyme disease 
MS 
Botulism
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83
Q

What is the pathological process involved in Guillain barre syndrome?

A

Post infective immune mediated

Antibodies that cross react with glycolipids and gangliosides distributed through myelin in peripheral nervous system

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84
Q

What investigations can be used to confirm guillain barre syndrome?

A

Nerve conduction studies: slowed conduction
LP: elevated CSF protein
LFT: elevated AST and ALT
Spirometry: reduced vital capacity, max inspiratory pressure
Antiganglioside antibody

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85
Q

What is the management for guillain barre syndrome?

A

IV immunoglobulin 400mg/kg/day for 5 days
Plasma exchange if IgA deficiency or renal failure
DVT prophylaxis
Intubation and ventilation
Gabapentin or carbamazepine for pain
Fluid boluses if hypotensive

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86
Q

What are the characteristic features of myasthenia gravis?

A

Skeletal muscle weakness

Increased fatigability

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87
Q

What thymus problems do people with myasthenia gravis have?

A

65% hyperplasia of thymus

12% thymoma

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88
Q

How do you treat myasthenia gravis?

A

Rest
Pyridostigmine - acetylecholinesterase inhibitor
Prednisolone
Azathioprine, mycophenolate or methotrexate
Thymectomy - 25% chance remission, 50% improve symptoms
Severe/life threatening - plasmapheresis, IV immunoglobulin

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89
Q

What is the charity which provides useful information and support to people living with myasthenia gravis?

A

Myaware

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90
Q

What are side effects of pyridostigmine?

A
Cholinergic crisis if overdose
Diarrhoea 
Urinary frequency
Meiosis 
Excessive salivation and lacrimation
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91
Q

What might cause a myasthenic crisis?

A

Drug omission
Infection
Stress

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92
Q

What are indications for an immediate CT head after head injury?

A

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
Post-traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting

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93
Q

What are indications for a CT head within 8 hours of head injury?

A

Adults with risk factors who have experienced loss of consciousness or amnesia since injury:
Age 65 years or older
Any history of bleeding or clotting disorders
Dangerous mechanism of injury (pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
More than 30 minutes’ retrograde amnesia of events immediately before the head injury
Patient on warfarin

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94
Q

Which nerve is at risk during a carotid endarterectomy procedure?

A

Ipsilateral hypoglossal

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95
Q

What haemodynamic combination is most likely to be seen prior to coning? What is this reflex called?

A

Hypertension and bradycardia

Cushing’s reflex - pre terminal event

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96
Q

What are causes of primary brain injury?

A

Focal: contusion, haematoma
Diffuse: diffuse axonal injury

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97
Q

What are causes of secondary brain injury?

A

Cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation

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98
Q

What are risk factors for subdural haematoma?

A

Old age
Alcoholism
Anticoagulation

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99
Q

A 22-year-old mechanic is involved in a fight. He is hit on the head with a hammer. On examination he had clinical evidence of an open depressed skull fracture and a GCS of 6/15. What imaging is indicated?

A

Urgent neurosurgical review (even before CT head performed)

GCS less than 8

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100
Q

A 67-year-old retired lawyer falls down the stairs. His GCS is 15/15 and he has some bruising over the mastoid. What imaging is indicated?

A

CT head within an hour

Basal skull fracture, indicated by a positive Battle’s sign

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101
Q

A 52-year-old secretary falls down ‘10-11’ stairs. She complains of neck pain. She has a GCS of 15/15 and no neurology. She is unable to rotate her c-spine 45 degrees to the left and right. What imaging is indicated?

A

C spine immobilisation and CT c spine

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102
Q

What is Kernigs sign?

A

Positive when the thigh is flexed at the hip and knee at 90-degree angles and subsequent extension of the knee elicits pain. This can be indicative of meningism of subarachnoid haemorrhage

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103
Q

An elderly patient with a precious history of spinal canal stenosis sustains an extension injury of the cervical spine. The upper limbs are more affected than the lower and perianal sensation is preserved. What is the likely diagnosis?

A

Central core syndrome - motor and sensory loss, upper limbs mainly

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104
Q

What are some causes of a spastic paraparesis?

A

Metastatic infiltration of the spine
Vascular disorders
Osteoporotic collapse of vertebrae

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105
Q

What are some causes of facial nerve palsy?

A

Intracranial: brain stem tumour, stroke, ms, acoustic neuroma
Intratemporal: otitis media, Ramsay hunt, cholesteatoma
Infratemporal: parotid tumour, trauma
Other: sarcoidosis, guillain barre, diabetes, Bell’s palsy

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106
Q

In a patient presenting with amaurosis fugax but is otherwise fit and well, what treatment should they be started on?

A

Clopidogrel 75mg od
OR
Aspirin 75mg od plus dipyridamole mr 200mg bd if intolerant to clopidogrel

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107
Q

In a patient presenting with amaurosis fugax and af, what treatment should they be started on?

A

Warfarin - stroke risk

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108
Q

What are the layers of the scalp?

A

S: Skin from which head hair grows. Contains numerous sebaeceous glands and hair follicles
C: Connective tissue. A dense subcutaneous layer of fat and fibrous tissue containing nerves and vessels
A: Aponeurosis (epicranial or galea aponeurotica). Tough layer of dense fibrous tissue which runs from frontalis anteriorly to occipitalis posteriorly
L: Loose areolar connective tissue layer, easy plane of separation between upper three layers and pericranium. Referred to as danger zone because of ease by which infectious agents can spread through it to emissary veins which drain into the cranium. Made up of collagen I, collagen III, glycosaminoglycans
P: Pericranium is the periosteum of skull bones and provides nutrition to bone and the capacity for repair

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109
Q

What is Hutchinson’s sign?

A

Vesicles on tip or side of the nose, precedes the development of ophthalmic herpes zoster - sight threatening
Nasociliary branch of the trigeminal nerve innervates both the cornea and the lateral dorsum of the nose as well as the tip of the nose

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110
Q

What is the Le Fort fracture classification?

A

Fractures of midface, which involve separation of all or a portion of the midface from the skull base. In order to be separated from the skull base the pterygoid plates of the sphenoid bone need to be involved as these connect the midface to the sphenoid bone dorsally
Le Fort 1 is a horizontal maxillary fracture, separating the teeth from the upper face (floating palate)
Le Fort 2 is a pyramidal fracture, with the teeth at the pyramid base, and nasofrontal suture at its apex (floating maxilla)
Le Fort 3 is craniofacial dysjunction (floating face)

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111
Q

What is the Monroe Kellie principle?

A

Pressure-volume relationship that aims to keep a dynamic equilibrium among the essential non-compressible components inside the rigid compartment of the skull
Average intracranial volume in an adult is around 1700 mL, composed of brain tissue (1400 mL), CSF (150 mL), and blood (150 mL). The volume of these three components remains nearly constant in a state of dynamic equilibrium. Thus, a decrease in one component should be compensated by the increase in other and vice-a-versa

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112
Q

What should be given to prevent vasospasm in a subarachnoid haemorrhage?

A

Nimodipine - CCB

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113
Q

What complications are we aiming to prevent in management of SAH?

A
Rebleeding
Vasospasm
Hydrocephalus
Hyponatraemia
Seizures
Acute pulmonary oedema
Cardiac dysfunction
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114
Q

What is the difference between a communicating and obstructive hydrocephalus?

A

Communicating: impaired cerebrospinal fluid reabsorption in absence of any CSF-flow obstruction between the ventricles and subarachnoid space - SAH, meningitis. Functional impairment of the arachnoidal granulations
Obstructive: CSF-flow obstruction. Foramen of Monro obstruction may lead to dilation of lateral ventricles
Aqueduct of Sylvius, normally narrow to begin with, may be obstructed and lead to dilation of both lateral ventricles as well as the third ventricle
Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the lateral and third ventricles
Foramina of Luschka and foramen of Magendie may be obstructed due to congenital malformation

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115
Q

How is brain stem death confirmed?

A

Preconditions: apnoeic coma, defined cause of severe and irreversible brain damage, core temperature above 34
Tests by 2 doctors, repeated
Fixed unresponsive pupils with absence of direct and consensual light reflexes
Absent corneal reflexes
Absent vestibulo ocular reflexes
Absent motor activity after painful stimuli
Absent gag reflex
Absent spontaneous respiration

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116
Q

What are causes of neck stiffness?

A

Meningitic conditions
Tumours
Subarachnoid haemorrhage
Bony abnormalities: cervical spondylosis

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117
Q

What are features of benign essential tremor?

A

Postural tremor worse if arms outstretched
Improved by alcohol and rest
Cause titubation

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118
Q

What is the management for essential tremor?

A

Propranolol

Primidone

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119
Q

What are the criteria for ABCD2 for prognosis in TIA?

A

Age > 60
Blood pressure >140/90
Clinical features: unilateral weakness (2), speech disturbance (1)
Duration of symptoms: >60 mins (2), 10-59 mins (1)
Diabetes

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120
Q

What does an ABCD2 score of 4 or above tell you?

A

Had TIA and are at higher risk of stroke
Need aspirin started immediately
Specialist assessment and investigations within 24 hours of symptoms
Secondary prevention

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121
Q

What needs to be done if an ABCD2 score is 3 or below?

A

Specialist assessment within 1 week of symptoms

If vascular territory or pathology uncertain, refer for imaging

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122
Q

What should be done with patients with crescendo TIAs? (Two or more episodes in a week

A

Treated as high risk of stroke even if ABCD2 score is 3 or less

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123
Q

Why does myeloma increase risk of stroke?

A

Paraproteinaemia - hyperviscosity of blood

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124
Q

Which drugs are used for migraine prophylaxis?

A

Topiramate or propranolol

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125
Q

Which migraine prophylaxis drug is preferable in a woman of child bearing age?

A

Propranolol preferable to topiramate due to teratogenic effects and reduced effectiveness of hormonal contraceptives

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126
Q

What is first line management for an acute migraine?

A

Combination therapy with oral triptan and NSAID/paracetamol

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127
Q

An 18 year old female presents with tremor and dysarthria, there is a family hx of early onset liver disease. Blood tests show a raised ALT. What is the most likely diagnosis?

A

Wilson’s disease

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128
Q

How is Wilson’s disease inherited?

A

Autosomal recessive

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129
Q

What is the defect in Wilson’s disease?

A

ATP7B gene on chromosome 13 leading to excessive copper deposition in tissues due to increased absorption and decreased hepatic excretion

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130
Q

What are features of Wilson’s disease?

A

Liver: hepatitis, cirrhosis
Neuro: basal ganglia degeneration, speech and behavioural problems, asterixis, chorea, dementia
Kayser-fletcher rings
Renal tubular acidosis (fanconi syndrome)
Haemolysis
Blue nails

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131
Q

How is a diagnosis of Wilson’s disease made?

A

Reduced serum caeruloplasmin
Reduced serum copper
Increase 24h urinary copper excretion

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132
Q

What is the management of Wilson’s disease?

A

Penicillamine (chelates copper)

Trientine hydrochloride

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133
Q

What is the preferred benzodiazepine to give IV in the presence of ongoing seizures?

A

Lorazepam

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134
Q

What is the preferred benzo to give in a child with ongoing seizures?

A

Buccal midazola,

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135
Q

What is the next line of management if seizures were to continue despite two doses of benzodiazepine?

A

Phenytoin

Senior help as intubation and ventilation may be required

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136
Q

What is Charcots triad in the context of MS?

A

Suggestive of cerebellar lesions in MS
Nystagmus
Intention tremor
Staccato speech

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137
Q

In a patient presenting with headache and amenorrhoea combined with some visual field loss, what needs to be investigated and how?

A

Pituitary lesion

Assessment of pituitary function, MRI and serum prolactin

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138
Q

What are the International Headache Society diagnostic criteria for migraine without aura?

A

At least 5 attacks fulfilling:
Headache lasting 4-72 hours
Headache that is: unilateral, pulsating, moderate to severe, aggravated by activity
During headache: nausea/vomiting, photo/phonophobia
Not attributed to another disorder

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139
Q

Give examples of typical auras that precede migraines

A

Transient hemianopic disturbance
Spreading scintillating scotoma (jagged crescent)
Develop over at least 5 mins and last 5-60 mins

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140
Q

What is the oxford stroke classification? (Bamford)

A

Total anterior circulation infarct: middle and anterior cerebral arteries. Hemiparaesis/hemisensory loss, homonymous hemianopia, higher cognitive dysfunction
Partial anterior circulation infarct: smaller artistes of anterior circulation. 2 of above criteria
Posterior circulation infarct: vertebrobasilar arteries. Cerebellar/brainstem syndromes, loss of consciousness, isolated homonymous hemianopia
Lacunar: perforating arteries around internal capsule, thalamus, basal ganglia. Unilateral weakness/sensory deficit, pure sensory, ataxic hemiparesis

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141
Q

What is lateral medullary syndrome?

A

Posterior inferior cerebellar artery stroke
Wallenbergs syndrome
Ipsilateral ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy - horners
Contralateral limb sensory loss

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142
Q

What is webers syndrome?

A

Ipsilateral III palsy

Contralateral weakness

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143
Q

Which conditions are associated with berry aneurysms?

A

Adult polycystic kidney disease
Ehlers-Danlos syndrome
Coarctation of the aorta

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144
Q

What are some causes of subarachnoid haemorrhage?

A

Berry aneurysm rupture
AV malformations
Trauma
Tumours

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145
Q

How should subarachnoid haemorrhage be investigated?

A

CT

Lumbar puncture after 12 hours (time for xanthochromia to develop)

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146
Q

What are complications of subarachnoid haemorrhage?

A

Rebleeding
Obstructive hydrocephalus
Vasospasm leading to cerebral ischaemia

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147
Q

What is the management of subarachnoid haemorrhage?

A

Neurosurgical opinion

Post op nimodipine 60mg/4h if BP allows

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148
Q

What is an Adie pupil?

A

Tonically dilated pupil
Slowly reactive to light with more definite accommodation response
Damage to parasympathetic innervation of eye due to viral or bacterial infection
Accompanied by absent knee or ankle jerks

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149
Q

What is a Marcus-Gunn pupil?

A

Relative afferent pupillary defect seen during swinging light examination
Pupil constricts less and therefore appears to dilate when like swung from unaffected to affected eye
Damage to optic nerve or severe retinal disease

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150
Q

What signs does horners produce?

A

Miosis (pupil constriction)
Ptosis (droopy eyelid)
Apparent enopthalmos
Anhydrosis

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151
Q

What is Hutchinsons pupil?

A

Unilaterally dilated pupil unresponsive to light

Compression of oculomotor nerve by intracranial mass

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152
Q

What is an Argyll Robertson pupil?

A

Bilaterally small pupils that accommodate but don’t react to bright light
Prostitutes pupil - neurosyphilis
Diabetic neuropathy

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153
Q

Which infection classically triggers Guillain Barre?

A

Campylobacter jejuni

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154
Q

What are characteristic features of Guillain Barre?

A

Progressive weakness of all 4 limbs, ascending
Proximal muscles before distal
Very few sensory signs
Areflexia
Cranial nerve involvement - diplopia
Autonomic involvement - urinary retention

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155
Q

Aneurysm where needs to be ruled out with an acute onset painful third nerve palsy?

A

Posterior communicating artery

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156
Q

Which type of motor neurone disease carries the worst prognosis?

A

Progressive bulbar palsy

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157
Q

What is the most common presentation of MS?

A

Optic neuritis

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158
Q

In which tubes from a lumbar puncture should red blood cell count be determined?

A

4 tubes altogether

RBC count in 1 and 4

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159
Q

What features of CSF suggest SAH?

A

Elevated opening pressure
RBC that does not diminish between tubes 1 and 4
Xanthochromia after 12 hours

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160
Q

What are the different forms of motor neurone disease?

A

Amyotrophic lateral sclerosis
Primary lateral sclerosis
Progressive muscular atrophy
Progressive bulbar palsy

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161
Q

What is a rosier scale assessment?

A
Differentiate patients with stroke and stroke mimics 
LOC -1
Seizure -1
Facial weakness +1
Arm weakness +1
Leg weakness +1
Speech disturbance +1
Visual field defect +1
Stroke likely if score >0
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162
Q

Which medications are associated with IIH?

A
Tetracycline antibiotics
Isotretinoin 
Contraceptives
Steroids
Levothyroxine
Lithium
Cimetidine
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163
Q

What are risk factors for IIH?

A

Obesity
Female
Pregnancy
Drugs: OCP, steroids, tetracycline, vit A, lithium

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164
Q

What are features of IIH?

A
Headache
Blurred vision 
Papilloedema
Enlarged blind spot
Sixth nerve palsy
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165
Q

What is the management of IIH?

A
Weight loss
Diuretics - acetazolamide 
Topiramate 
Repeated lumbar puncture
Surgery - optic nerve sheath decompression and fenestration, lumboperitoneal or ventriculoperitoneal shunt
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166
Q

In a patient with a stroke and AF with a slow ventricular response, what is the management?

A

Aspirin 300mg OD for 2 weeks then lifelong anti coagulation

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167
Q

Where is the lesion which leads to hemiballismus?

A

Contralateral subthalamic nucleus

168
Q

What are some causes of hemiballismus?

A
Stroke
Traumatic brain injury
Amyotrophic lateral sclerosis 
Hyperglycaemia 
Malignancy
Vascular malformations
Tuberculomas 
Demyelinating plaques
169
Q

What are features of Wilson’s disease?

A
Liver: hepatitis, cirrhosis
Neuro: basal ganglia degeneration, speech and behavioural problems, asterixis, chorea, dementia
Kayser fletcher rings 
Renal tubular acidosis 
Haemolysis
Blue nails
170
Q

How is wilsons inherited?

A

Autosomal recessive

171
Q

What are the underlying problems in Wilson’s disease?

A

Increased copper absorption from small intestine
Decreased hepatic copper excretion
Defect in ATP7B gene on chromosome 13

172
Q

How is Wilson’s disease diagnosed?

A

Reduced serum caeruloplasmin
Reduced serum copper
Increased 24h urinary copper excretion

173
Q

How is Wilson’s disease managed?

A

Penicillamine (copper chelator)

Trientine hydrochloride

174
Q

Which nerve is at risk in saphenopopliteal ligation for varicose veins?

A

Common peroneal nerve

175
Q

What is the difference between simple and complex partial seizures?

A

Simple: no disturbance of consciousness
Complex: consciousness disturbed

176
Q

What are presenting features of MS?

A
Spastic paraparesis
Cerebellar signs
Optic atrophy
Nystagmus
Internuclear opthalmoplegia 
Urinary incontinence
177
Q

What does CSF examination show in MS?

A

Raised protein and lymphocyte count
Oligoclonal bands of IgG on electrophoresis
Delayed visual, auditory and somatosensory evoked potentials

178
Q

What is transient global amnesia?

A

Transient vascular insufficiency of both hippocampi
Usually affects people over 50
Lasts less than 24h
Awareness of personal identity is retained, along with normal cognition

179
Q

How can the weakness in lambert eaton myasthenia be differentiated from that of myasthenia gravis?

A

Lambert eaton: weakness affects legs more than arms, gets better with exertion
Myasthenia: weakness arms more than legs, gets worse on exertion, easily fatigued

180
Q

Which nerve root is likely damaged with weakness of ankle dorsiflexion, eversion and inversion, decreased ankle jerk and sensory loss confined to dorsum of the foot and anterior leg?

A

L5

181
Q

What are features of neuroleptic malignant syndrome? Which neurotransmitters/brain regions are responsible for each symptom?

A
Muscle rigidity - dopamine 
Parkinsonism - dopamine 
Tremor - dopamine 
Hyperreflexia - calcium 
Rhabdomyolysis - calcium 
Renal failure - calcium 
Agitation - mesolimbic system 
Confusion - reticular activating system 
Labile blood pressure - dopamine 
Tachycardia - dopamine 
Pyrexia 
Sweating 
White cell count raised
182
Q

What is the management of neuroleptic malignant syndrome?

A

IV fluids
Dantrolene (Ryanodine receptor antagonist)
Bromocriptine (dopamine agonist)

183
Q

What are some adverse effects of sodium valproate?

A
Nausea
Increased appetite and weight gain
Alopecia 
Ataxia
Tremor
Hepatitis
Pancreatitis
Thrombocytopenia 
Teratogenic
Hyponatraemia
184
Q

What are important factors required for a diagnosis of dementia?

A

Two or more cognitive impairments, one being memory
Sufficiently effected to cause functional impairment
No physical abnormality effecting cognition
Patient fully alert when assessed

185
Q

How is dementia staged?

A

Mild: difficulties with ADLs, score over 23
Moderate: unable to manage independent living, score 11 to 22
Severe: personal ADLs severely impaired, score under 10

186
Q

What is the triad of symptoms for wernickes?

A

Confusion
Ataxia
Opthalmoplegia

187
Q

What is the treatment for wernickes?

A

IV high potency 2-3 pairs TDS for 2 days

188
Q

What is a tensilon test?

A

Diagnosis of myasthenia gravis

Administration of intravenous edrophonium rapidly reverses symptoms

189
Q

Why is a diabetic 3rd nerve palsy painful?

A

Infarction of the nerve

190
Q

What are features of cavernous sinus syndrome?

A

Opthalmoplegia
Pain
Proptosis
Prominent vessels

191
Q

What is the treatment for Huntingtons and other hyperkinetic movement disorders?

A

Tetrabenazine - depletes dopamine

192
Q

What are causes of optic neuritis?

A

MS
Diabetes
Syphilis

193
Q

What are features of optic neuritis?

A

Unilateral decrease in visual acuity over hours or days
Poor discrimination of colours - red desaturation
Pain worse on eye movement
Relative afferent pupillary defect
Central scotoma

194
Q

What is the management for optic neuritis?

A

High dose steroids

195
Q

What is Hoffmans sign?

A

Flicking the distal phalanx of the middle finger to cause momentary flexion
Positive result is exaggerated flexion of the terminal phalanx of the thumb
Sign of upper motor neuron lesion

196
Q

What is a tensilon test?

A

Tensilon is an anticholinesterase inhibitor

People with myaesthenia gravis get stronger when injected with tensilon

197
Q

What is bulbar palsy? What are clinical features?

A

Lower motor neurone lesion of cranial nerve 9-12

Tongue flaccid and fasciculating, dysarthria, absent palatal movement, bovine cough, dysphagia, nasal regurgitation

198
Q

What are some causes of bulbar palsy?

A
Motor neurone disease
Syringobulbia 
Guillain Barre syndrome
Poliomyelitis
Neuro syphilis
199
Q

What are some indications for an urgent CT head? (Within 1 hour)

A

GCS <13 on initial assessment
GCS <15 at 2 hours post injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture: haemotympanum, panda eyes, csb rhinorrhoea, battles sign
Post traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting

200
Q

What are some indications for CT head within 8 hours of head injury?

A

Adults who have had a LOC or amnesia since injury and have any of these risk factors:
Over 65
History of bleeding or clotting disorder
Dangerous mechanism of injury: pedestrian hit by car, ejected from motor vehicle, fall from height greater than 1m or 5 stairs
More than 30 mins retrograde amnesia of events immediately before the injury
Patient on warfarin

201
Q

What are features of myotonic dystrophy?

A

Frontal baldness
Atrophy of temporalis, masseters and facial muscle
Neck muscle atrophy
Cardiac abnormalities: first degree heart block, complete heart block

202
Q

How does subclavian steal syndrome present?

A

Posterior circulation problems such as dizziness or vertigo during exertion of an arm

203
Q

What is subclavian steal syndrome?

A

Subclavian artery steno occlusive disease proximal to origin of vertebral artery
Flow reversal in vertebral artery

204
Q

What is a stroke?

A

Rapidly developing clinical signs of focal disturbance of cerebral function, lasting more than 24 hours or leading to death

205
Q

What is the most common cause of stroke?

A

Arterial embolism or thrombus

206
Q

What is the most common cause of stroke in younger adults?

A

Carotid or vertebral artery dissection

207
Q

Which scoring systems are used in TIA and stroke?

A

ABCD2 in TIA

ROSIER in Stroke

208
Q

What are the categories of the ABCD2 score?

A

A – Age >60 years – 1 pt
B – Initial BP reading either SBP >140 or DBP >90 - 1 pt
C – Clinical features of TIA, Unilateral weakness – 2pts, Speech disturbance without weakness – 1pt
D – Duration of symptoms 10-59 minutes – 1pt, >60 minutes – 2 pts
D – Diabetes – 1pt

209
Q

Which TIAs are considered high risk?

A
ABCD2 score >4 
Crescendo TIA (2 or more TIAs in 1 week)
210
Q

How is a high risk TIA managed?

A
Aspirin 300mg daily 
Specialist assessment and investigation within 24hr
Make decision on brain imaging – MRI 
Carotid imaging, endarterectomy 
Secondary prevention
211
Q

What are the different categories of stroke?

A

Cerebral hemispheric infarcts: Total/partial Anterior circulation infarction (TACI/PACI)
Brainstem infarcts: Posterior circulation infarct (POCI)
Lacunar: Lacunar infarct (LACI)

212
Q

What are the clinical features of total anterior circulation syndrome/infarct?

A

All 3 of:
Unilateral weakness +/- sensory deficit
Higher dysfunction (dysphasia)
Homonymous hemianopia

213
Q

How does a partial anterior circulation syndrome/infarct present?

A

2 of:
Unilateral weakness +/- sensory deficit
Higher dysfunction (dysphasia)
Homonymous hemianopia

214
Q

What are features of a posterior circulation syndrome/infarct?

A

1 of:
Cerebellar/ brainstem syndromes: DANISH
LOC
Isolated homonymous hemianopia

215
Q

How can lacunar infarcts present?

A

Pure motor hemiparesis – contralateral weakness of face, arm and leg with no sensory deficit
Pure sensory stroke – involving contralateral half of body
Dysarthria
Ataxic hemiparesis – on ipsilateral side

216
Q

What are indications for immediate imaging in acute stroke?

A

Thrombolysis indicated
On anticoagulation
Bleeding tendency
Reduced GCS
Unexplained progressive or fluctuating symptoms
Papilloedema, neck stiffness or fever
Severe headache at onset of stroke symptoms

217
Q

What is the management of acute stroke?

A

Thrombolysis with Alteplase: exclusion criteria
Aspirin 300mg (oral or rectally if dysphagic) - for 2 weeks
Homeostasis: O2 if SpO2 <95%, BM maintained between 4-11 mmol/L, Lower BP only if hypertensive emergency, <185/110 mmHg if for thrombolysis
Swallow assessment – need for NG
Dietician input
Early mobilisation when able
Surgical referral for acute intracerebral haemorrhage

218
Q

What is multiple sclerosis?

A

Autoimmune demyelinating disease of the CNS characterised by repeated episodes of inflammation leading to reduced signal transmission

219
Q

What are the patterns of MS?

A

Relapsing-remitting – symptoms come and go
Secondary progressive – follows on from relapsing-remitting - gradually worsening of symptoms with fewer remissions
Primary progressive – gradually worsening of symptoms from onset
Clinically isolated syndrome

220
Q

What are signs and symptoms of MS?

A

Sensory symptoms of limbs and face
Unilateral visual loss with painful eye movements
Motor weakness
Diplopia
Balance problems (unsteadiness, clumsiness)
Lhermitte’s sign (electric shock down spine triggered by bending head forward)
Autonomic dysfunction

221
Q

How should MS be investigated?

A
Exclusion of differentials 
Standard bloods – inflammatory markers (ESR, CRP), LFTs, U&amp;Es
HIV serology in at risk groups 
B12 
Calcium 
Referral to a consultant Neurologist 
Electrophysiology 
MRI – 95% periventricular lesions / white matter abnormalities
222
Q

How is a diagnosis of MS made?

A

McDonald Criteria
Takes into account number of attacks and evidence of lesions on MRI (lesions at different times and different anatomical locations)
Dissemination in time and space

223
Q

What is the management of MS?

A
Support (medical/social) - advance care planning
Lifestyle advice 
Methylprednisolone for relapses 
Disease modifying therapy 
Interferon – no longer recommended 
Dimethyl fumarate (relapsing-remitting)
Management of general symptoms: Fatigue, Pain - neuropathic, Visual problems 
Physio and occupational therapy
224
Q

What is motor neurone disease?

A

Destruction of anterior horn cells of the spinal cord and motor cranial nuclei
Leading to upper and lower motor neuron dysfunction

225
Q

What are clinical features of motor neurone disease?

A

Limb weakness – wasting, fasciculations (thighs), distal weakness
Bulbar involvement – wasting and fasciculations of tongue
Respiratory involvement
Absence of major sensory symptoms and pain

226
Q

What are the clinical patterns of motor neurone disease?

A

Amylotrophic lateral sclerosis: Combination of lateral corticospinal tracts and anterior horn cell disease, Progressive spastic tetraparesis, Combination UMN and LMN
Progressive muscular atrophy: Predominantly LMN lesion of the cord, weakness, wasting, fasciculations, Leading to UMN signs later in course (2 years)
Progressive bulbar palsy: UMN and LMN disorder of cranial muscles, Dysarthria and dysphagia
Primary lateral sclerosis: Isolated UMN, Slower progression

227
Q

How does MND typically present?

A

Loss of dexterity, falls, trips
Speech or swallowing problems (bulbar presentation)
Muscular weakness, wasting, twitching, cramps, stiffness
Breathing problems and effects of reduced respiratory function: Orthopnea, Fatigue, Morning headache
Cognitive features

228
Q

What is the management of MND?

A

No specific investigations – electrophysiology may show characteristic pattern of fibrillations and fasciculation’s
MDT approach
Respiratory function testing: SpO2 – at rest on room air plus Measurement of FVC
SpO2 of 92-94% on room air then do ABG for assessment of pCO2 and need for ventilatory support: NIV

229
Q

What usually causes death in patients with motor neurone disease?

A

respiratory failure

230
Q

What is the median survival of patients with motor neurone disease?

A

2-4 years

231
Q

What is degenerative cervical myelopathy?

A

Cervical spinal cord compression due to cervical spondylosis

232
Q

What is the most common cause of non traumatic tetraparesis in developed countries?

A

Degenerative cervical myelopathy

233
Q

What is the name of the disability score used in MS?

A

Kurtzke scale

234
Q

What features would support a diagnosis of Korsakoff’s syndrome?

A

Anterograde amnesia
Confabulation
Lack of insight
Chronic alcoholism

235
Q

What is brown sequard syndrome and how does it present?

A

Hemi-section of the cord / lateral injury of the cord
Ipsilateral spastic paresis and loss of proprioception and vibration sense
Contralateral loss of pain and temperature

236
Q

What is guillain barre and how does it present?

A

Demyelination and axonal degeneration
Ascending pattern of progressive symmetricalweakness
Usually 3 weeks after viral illness (resp / GI)
Sensory symptoms may be present

237
Q

What is Webers syndrome?

A

Midbrain stroke the involves fascicles of the oculomotor nerve resulting in ipsilateral cranial nerve 3 palsy and contralateral hemiplegia

238
Q

Which medications can be used for migraine prophylaxis?

A

Topiramate

Propranolol

239
Q

Which medications should be used in an acute migraine attack?

A

Triptan
NSAID
Paracetamol

240
Q

In which patients should migraine prophylaxis be offered?

A

2 or more attacks per month producing disability lasting 3 days or more

241
Q

What should be offered for migraines if propranolol/topiramate fail as prophylaxis?

A

A course of up to 10 sessions of acupuncture over 5-8 weeks

Gabapentin

242
Q

What is a shagreen patch?

A

Roughened area of skin found in tuberous sclerosis

243
Q

How can you differentiate between myasthenia gravis and lambert eaton?

A

Myasthenia gravis: weakness worsens with exercise

Lambert eaton: weakness improves with exercise

244
Q

How does lateral medullary syndrome present?

A
Vertigo with vomiting
Dysphagia 
Nystagmus on looking to side of lesion
Ipsilateral hypotonia 
Ataxia
Horners syndrome
Paralysis of soft palate 
Dissociated sensory loss
245
Q

What are features of myotonic dystrophy?

A
Muscle weakness 
Myotonia 
Ptosis 
Frontal balding
Cataracts
Cardiomyopathy 
Impaired intellect
Testicular atrophy
Diabetes mellitus
Dysarthria
246
Q

What does a patient with Alzheimer’s need to do with regards their driving?

A

Attend a driving assessment centre

247
Q

For how long does a patient with first attack idiopathic epilepsy need to stop driving?

A

Fit free for 6 months

248
Q

What are differential diagnoses for ring enhancing lesions in the brain?

A
Cerebral mets
Toxoplasmosis
Histoplasmosis
Abscess
Some primary brain tumours
249
Q

What is miller fisher variant of guillain barre syndrome?

A

Starts by affecting cranial nerves
Manifests with eye signs - opthalmoplegia, areflexia and ataxia
Tend to be preceded by an infection - campylobacter jejuni

250
Q

After what time period should anticoagulation start in patients with ischaemic stroke with AF?

A

14 days after onset - risk of secondary haemorrhage in early phase

251
Q

What are absolute contraindications to thrombolysis?

A
Previous intracranial haemorrhage
Seizure at onset stroke
Intracranial neoplasm
Suspected SAH
Stroke or traumatic brain injury in previous 3 months
Lumbar puncture in previous 7 days
GI bleed in previous 3 weeks
Active bleeding
Pregnancy 
Oesophageal varices
Uncontrolled HTN >200/120
252
Q

What are relative contraindications to thrombolysis?

A
Concurrent anticoagulation INR >1.7
Haemorrhagic diathesis
Active diabetic haemorrhagic retinopathy
Suspected intracardiac thrombus
Major surgery/ trauma in past 2 weeks
253
Q

What is the appropriate management for a patient identified to have degenerative cervical myelopathy?

A

Cervical decompressive surgery

254
Q

Why does hypocalcaemia cause tetany?

A

Low extracellular calcium increases permeability of neuronal membranes to sodium, causing progressive depolarisation which increases possibility of action potentials

255
Q

What is shy drager syndrome?

A

Type of multiple system atrophy

256
Q

What are features of cavernous sinus syndrome?

A
Pain
Opthalmoplegia 
Proptosis 
Trigeminal nerve lesion (opthalmic branch)
Horners syndrome
257
Q

What are features of multiple system atrophy?

A

Parkinsonism
Autonomic disturbance: atonic bladder, postural hypotension
Cerebellar signs

258
Q

What are criteria for migraine without aura?

A

A: at least 5 points fulfilling criteria B-D
B: headache lasting 4-72 hours
C: headache with 2 of- unilateral, pulsating, moderate/severe, aggravated by or causing avoidance of routine
D: nausea/vomiting, photophobia, phonophobia
E: not attributed to another disorder

259
Q

With which virus is nasopharyngeal carcinoma associated?

A

EBV

260
Q

Why are spinal discs so much more likely to herniate posteriolaterally rather than directly posterior?

A

Posterior longitudinal ligament

261
Q

Which blood tests are involved in a confusion screen?

A
FBC 
U and Es
LFTs 
INR
TFTs
Calcium
B12/folate/haematinics
Glucose 
Blood cultures if suspicion of sepsis
262
Q

What factors can trigger migraines?

A
Hormone changes 
Stress
Certain foods: cheese, aspartame, MSG
Alcohol
Sensory stimuli 
Changes to sleep pattern
Physical exertion
Weather changes 
COCP
263
Q

What are features of lateral medullary syndrome?

A
Ipsilateral ataxia
Nystagmus
Dysphagia 
Facial numbness
Cranial nerve palsy 
Contralateral hemisensory loss
264
Q

What is Bell’s palsy?

A

Acute unilateral idiopathic facial nerve paralysis
Peak incidence 20-40 years
More common in pregnancy

265
Q

What are features of Bell’s palsy?

A
Lower motor neurone facial palsy, forehead affected 
Post auricular pain 
Altered taste
Dry eyes
Hyperacusis
266
Q

What is the management of Bell’s palsy?

A

Prednisolone 1mg/kg for 10 days within 72 hours of onset

Eye care: artificial tears and eye lubricant

267
Q

Describe the pathophysiology of papilloedema?

A

Axoplasmic flow stasis with intraaxonal oedema
Subarachnoid space of brain continuous with optic sheath
As CSF pressure increases, pressure is transmitted to optic nerve
Sheath acts as a tourniquet to impede axoplasmic transport

268
Q

Which conditions are associated with a waddling gait?

A

Proximal myopathy - osteomalacia, diabetic amyotropy
Cushing’s syndrome
Polymyositis
Metabolic derangements

269
Q

What antiplatelets should be given when a patient has an acute stroke?

A

Aspirin 300mg daily for 2 weeks
Clopidogrel 75mg daily long term
Statin if not on one

270
Q

What is an epileptic seizure?

A

A transient occurrence of signs and/or symptoms, the result of a primary change to the electrical activity (abnormally excessive or synchronous) in the brain

271
Q

What is epilepsy?

A

A condition in which a person is prone to recurrent epileptic seizures

272
Q

What is an epilepsy syndrome?

A

A distinctive disorder identifiable on the basis of a typical age of onset, seizure types, specific EEG characteristics, and often other features. Identification of epilepsy syndrome has implications for treatment, management and prognosis

273
Q

What is status epilepticus?

A

When a convulsive seizure continues for a prolonged period (longer than 30 minutes), or when convulsive seizures occur one after the other with no recovery between. Convulsive status epilepticus is an emergency and requires immediate medical attention

274
Q

What is SUDEP (sudden unexpected death in epilepsy)?

A

Sudden, unexplained, witnessed or unwitnessed, non-traumatic and non-drowning death in people with epilepsy, with or without evidence for a seizure, and excluding documented status epilepticus, in which post-mortem examination does not reveal a toxicological or anatomic cause for death

275
Q

What is non epileptic attack disorder (NEAD)?

A

A disorder characterised by episodes of change in behaviour or movement, not caused by a primary change in electrical activity of the brain. Movements are varied, and the attacks can be difficult to differentiate from epileptic seizures

276
Q

What are differential diagnoses for the cause of a seizure?

A
Epileptic seizure 
Hypoglycaemia
CNS infection: meningitis, encephalitis, cerebral abscess, TB, malaria
Febrile convulsion
Trauma/head injury
Child abuse
Raised intracranial pressure: tumour
Recreational drug use or poisoning or self-harm (overdose)
277
Q

What is the most common cause of neonatal seizures?

A

Hypoxic ischaemic encephalopathy

278
Q

What are causes of neonatal seizures?

A

Hypoxic ischaemic encephalopathy
Intracranial haemorrhage
Metabolic disturbance: hypoglycaemia, drug withdrawal
TORCH infection
Malformation of cortical development
Benign neonatal or infantile familial convulsions

279
Q

Why can damage occur to the brain in epilepsy?

A

The underlying disease
Systemic complications of the convulsions especially hypoxia from airway obstruction and later acidosis when systemic hypotension occurs
Direct injury from repetitive neuronal discharge
Increased cerebral metabolism by a factor of 3
Initially increased sympathetic activity with release of catecholamines
which leads to peripheral vasoconstriction and increased systemic blood pressure
There is loss of cerebral arterial regulation and consequential increase in cerebral blood flow
If fits continue, systemic blood pressure falls which leads to fall in cerebral blood flow
Lactic acid accumulates with subsequent cell death, oedema, free radical release, mitochondrial dysfunction and increased ICP which leads to worsening of cerebral perfusion
This associated with loss of systemic compensatory mechanisms with
resulting biochemical, renal, hepatic and cardiac failure

280
Q

What are complications of status epilepticus?

A
Airway obstruction 
Hypoxia 
Aspiration
Respiratory depression secondary to excess benzodiazepines
Cardiac arrhythmias
Pulmonary oedema
Hyperthermia
Hypertension
Disseminated intravascular coagulation (DIC)
281
Q

What are risk factors for the development of SUDEP?

A
Frequent seizures
Long epilepsy duration
Young adults
Early epilepsy onset
Lack of AED use
Subtherapeutic levels
Polytherapy >3 drugs
>2 AED changes per year
Rapid AED withdrawal
282
Q

What are red flags for headache?

A

Worsening headache with fever
Sudden-onset headache reaching maximum intensity within 5 minutes
New-onset neurological deficit
New-onset cognitive dysfunction
Change in personality
Impaired level of consciousness
Recent head trauma
Headache triggered by cough, valsalva or sneeze
Headache triggered by exercise
Orthostatic headache
Symptoms suggestive of giant cell arteritis
Symptoms and signs of acute angle closure glaucoma
Substantial change in the characteristics of their headache

283
Q

What is cerebral palsy?

A

Neurological disorder caused by a non-progressive brain
injury or malformation that occurs while the child’s brain is under development. Primarily affects body movement and
muscle coordination

284
Q

What are the different types of cerebral palsy?

A

Spastic: hemiplegia, diplegia, quadriplegia
Athetoid
Dyskinetic
Ataxic

285
Q

Which key professionals might need to be involved in the care of a child with cerebral palsy?

A
Health visitor and GP
Community Paediatrician/ Paediatric neurology
AHPs- OT, Physio, SALT
Orthopaedic surgeon/Spinal surgeon
Ophthalmology
Maxillofacial surgery
Community Nursing team
Educational Psychology
Special school
Social care
Respite services
Wheelchair services
Housing organisations
Family Fund and other charities
Youth services
286
Q

When should treatment for epilepsy be commenced?

A

2 or more unprovoked seizures

287
Q

Why is it important to classify epilepsy syndromes?

A

Determines choice of drug
Need for investigations
Prognosis

288
Q

Which is the most common form of adult epilepsy?

A

Focal (partial) onset syndromes

289
Q

What are the 3 main mechanisms of action of anti epileptic drugs?

A

Modulation of voltage gated ion channels: sodium, calcium
Enhancement of GABA mediated inhibitory neurotransmission
Decrease of glutamate mediated excitatory neurotransmission

290
Q

Which are first line AEDs for generalised onset seizures?

A

Sodium valproate if male
Lamotrigine
Topiramate
Levetiracetam

291
Q

Which are first line AEDs for focal onset seizures?

A

Carbamazepine
Lamotrigine
Levetiracetam
Topiramate

292
Q

Which drugs can interact with carbamazepine?

A

OCP, warfarin, antispychotics,antidepressants, other AEDs, erythromycin

293
Q

What is the main mechanism of action of carbamazepine?

A

inhibition of voltage-dependent Na conductance

294
Q

What is autoinduction which occurs with carbamazepine?

A

Marked increase in clearance and drop in serum half-life in the first few weeks of therapy; auto-induction finished after 1 month

295
Q

In which conditions is carbamazepine contraindicated?

A

AV conduction abnormalities, porphyria

296
Q

What are adverse effects of carbamazepine?

A
5-10% skin rash
Nausea, headache, ataxia, diplopia
Hyponatraemia
Leucopenia
Rare: SJS, Haematological; thrombocytopenia, pancytopenia– Hepatotoxicity
297
Q

What is the mechanism of action of lamotrigine?

A

Inhibition of Na channel conductance and block release glutamate

298
Q

What are side effects of lamotrigine?

A
Headache
Nausea
Dizziness
Diplopia
Ataxia
Rash 3% approx (if started too quickly)
GI symptoms
Rarely behavioural change
Rare: Hypersensitivity syndrome, SJS, Aplastic anaemia
299
Q

Which AED are strong enzyme inducers?

A

Carbamazepine
Phenytoin
Phenobarbitone
Primidone

300
Q

What is the main mechanism of action of sodium valproate?

A

Effects on GABA and glutamergic activity, and calcium and potassium conductance

301
Q

In which conditions is sodium valproate contraindicated?

A

Acute liver disease, porphyria

302
Q

What are common side effects of sodium valproate?

A
Weight gain
Hair loss
Tremor
GI SE
PCOS
Teratogenic effects
Rare: Hepatotoxicity, Encephalopathy, Pancreatitis, thrombocytopenia
303
Q

Which AEDs are category 1? What does that mean?

A

Phenytoin, carbamazepine, phenobarbital, primidone

Specific measures are necessary to ensure consistent supply of a particular product

304
Q

What is the mechanism of action of phenytoin?

A

Inhibition of voltage dependent Na channels

305
Q

What are contraindications to phenytoin?

A

Sinus bradycardia
Sinoatrial node block
2nd and 3rd degree heartblock
Porphyria

306
Q

What are possible IV side effects pf phenytoin?

A
Hypotension
Arrhythmias – especially prolonged QT
Thrombophlebitis at injection site
Purple glove syndrome – hand damage distal to injection site
Agranulocytosis
307
Q

What are common side effects of oral phenytoin?

A
Rash 5%
Acute toxicity: lethargy, ataxia, dysarthria
Gum hypertrophy
Coarsening of face, hirsutism, acne
Macrocytosis, leucopenia
Mental slowing, drowsiness
308
Q

What are potential long term consequences of phenytoin?

A

Cerebellar ataxia and cerebellar atrophy
Peripheral neuropathy
Osteoporosis
Folate deficiency and megalobalstic anaemia

309
Q

What are side effects of phenobarbitone?

A

Sedation and cognitive side effects
Reduction of folate levels
Connective tissue (frozen shoulder, plantar fibromatosis)
Rash
Rare: Ataxia, Osteomalacia, Megaloblastic anaemia, Neuropathy

310
Q

How long should a patient be seizure free before they can consider coming off anti epileptic drugs?

A

Eligible for coming off medication - seizure free for 2 years minimum

311
Q

What are indications for monitoring drug levels of antiepileptic drugs?

A
Non-adherence
Suspected toxicity 
Adjustment of phenytoin dose 
Management of interactions 
Specific clinical conditions. (organfailure, pregnancy, status epilepticus, interactions eg with NG feed)
312
Q

Who is at increased risk of epilepsy relapse after coming off AEDs?

A

Epilepsy since childhood
Patients who require more than one drug to control epilepsy
Had seizures while on medication
Suffered myoclonic or tonic-clonic seizures
Had an abnormal EEG in remission
Have known underlying brain damage

313
Q

What are rules on driving while coming off AEDs?

A

DVLA recommends that patients do not drive during drug withdrawal and for 6 months following withdrawal

314
Q

What are the criteria for diagnosis of Alzheimer’s?

A

Two or more than two cognitive impairments one being memory
Sufficiently effected to cause functional impairment
No other abnormality effecting cognition
Patient fully alert when assessed

315
Q

What are the different stages of Alzheimer’s?

A

MILD: Difficulties with IADL’s , score over 23
MODERATE : Unable to manage independent living : score 11 to 22.
SEVERE : PADL’s severely impaired. Score under 10

316
Q

What is mild cognitive impairment?

A

Clinically difficulties with new information,as a result slow, take longer but manage functional responsibilities

317
Q

What are different types of dementia?

A

Cortical : Alzheimer’s Disease, Pick’s Disease (Frontotemporal Dementia), Frontal Dementias
Sub-cortical Dementias: Extrapyramidal Syndromes (Parkinson’s
Disease, Huntington’s Disease, Progressive supranuclear palsy, Wilsons Disease, Spinocerebellar degeneration, Idiopathic basal ganglia calcification)
Hydrocephalus
White Mater Diseases: Small vessel disease, (Binswanger’s Disease), Multiple Sclerosis, HIV encephalopathy
Multi Infarct dementias
Infectious dementias
Toxic and metabolic encephalopathies, systemic illnesses, Endocrinopathies,
Deficiency states, Drug intoxications, Heavy metal exposure
Miscellaneous: Post traumatic, Post anoxic, Neoplastic

318
Q

What investigations should be done for suspected dementia?

A

Base Line: FBC, U and Es, LFTs, TFTs, Vitamin B12 and Folate, Glucose, Lipid Profile
Specific: Syphilis Serology, CSF, Serum copper
EEG
Brain Scanning: Structural (CT, MRI), Functional (FDG PET, FMRI, Amyloid )

319
Q

Why are older people more at risk of delirium?

A

Ageing or disease of the brain
Impairment of vision and hearing
Changes in pharmacokinetics and dynamics of drugs
High prevalence of chronic diseases.
High susceptibility to acute diseases
Reduced capacity for homeostatic regulation

320
Q

What are some non neuro complications of Parkinson’s disease?

A

Constipation, pain, urinary dysfunction, dysphagia, drooling, speech problems, depression, anxiety, dementia, psychosis, sexual dysfunction, sleep disturbance, orthostatic hypotension and hyposmia

321
Q

What are the clinical stages of Parkinson’s disease?

A

Diagnosis: recognition, treatment initiated
Maintenance: monitor symptoms, avoid complications
Complex: motor fluctuations, drug side effects, non motor symptoms, falls
Palliative: reduced efficacy of treatment, QOL/end of life issues

322
Q

What motor fluctuations can occur in the complex stage of Parkinson’s disease?

A

Freezing: Common during “offs” but can also occur when “on”
Wearing off: End of dose deterioration (motor and non motor), May be predictable or unpredictable, sudden or gradual
On and Off phenomena
Delayed “on” or no “on” (ie dose failures)
Dyskinesia: fidgety, wriggly snake like movements
Dystonia: May occur off (wearing off, early morning) but can occur at peak of dose, Painful

323
Q

What is the striatum?

A

Caudate nucleus and the putamen which are separated by the internal capsule

324
Q

What is the function of the striatum?

A

Responsible for bringing together the dopamine signals

from the substantia nigra with the voluntary movement signals from the prefrontal cortex

325
Q

What classes of drugs can be used to treat Parkinson’s?

A
Levodopa/carbidopa
Dopamine agonists
MAO-B inhibitors
COMT inhibitors
Amantadine
Continuous dopaminergic stimulation (CDS)
Acetylcholinesterase inhibitors
326
Q

What are the 2 main preparations of levodopa used for Parkinson’s?

A

Sinemet (carbidopa) co-careldopa

Madopar (benserazide) co-beneldopa

327
Q

What are some short term side effects of levodopa?

A

GI: N and V, Loss of appetite
Cardiovascular: Postural hypotension
Sleep: Somnolence, Insomnia, Vivid dreams, nightmares, Inversion of sleep-wake cycle
Psychiatric: Confusion, Visual hallucinations, Delusions, illusions

328
Q

What are some long term side effects of levodopa?

A

Involuntary movements: Peak-dose dyskinesia, Diphasic dyskinesia, Dystonia
Response fluctuations: Wearing off, Unpredictable on/off
Psychiatric: Confusion, Visual hallucinations, Delusions, illusions

329
Q

What are side effects of MAOIB drugs such as selegiline?

A

Hallucinations, insomnia, nightmares, vivid dreams

Postural hypotension, nausea, confusion

330
Q

What are some benefits of using rasagaline alongside other Parkinson’s drugs?

A

Reduces off time by 48-56 mins/day
Increases on time without dyskinesias
Similar in efficacy and tolerability to entacapone

331
Q

What are some problems with ergot derived dopamine agonists like bromocriptine, pergolide and carbergoline?

A

Cardiac valvulopathy

Pulmonary, retroperitoneal, and pericardial fibrotic reactions

332
Q

What are some common side effects of dopamine agonists?

A
N and V, loss of appetite
Postural hypotension
Confusion, hallucinations
Somnolence 
Impulse control disorders in up to 20%
333
Q

What are some examples of dopamine agonists used in Parkinson’s?

A

Ropinirole
Pramipexole
Rotigotine patch
Apomorphine s/c

334
Q

What are side effects of COMT inhibitors?

A
Dyskinesia (so decrease levodopa)
Diarrhoea
Nausea
Somnolence
Abdo pain
Discoloured urine (body fluids orange)
Hepatic toxicity (tolcapone): Rigorous blood monitoring, Stop if AST or ALT exceed upper limit of normal
335
Q

What forms of continuous dopaminergic stimulation are available for Parkinson’s?

A

Apomorphine
Duodopa
Deep brain stimulation

336
Q

Which drugs are usually used in early Parkinson’s disease?

A

Dopamine agonist
Levodopa
MAO B inhibitors

337
Q

What can be causes of confusion and agitation in a Parkinson’s disease patient?

A

Co-morbid medical illness (especially infection, metabolic upset)
Side-effects of the PD medication itself
Progression of Parkinson’s disease (development of PD dementia)

338
Q

What can be used to manage confusion and agitation in Parkinson’s disease?

A
Lorazepam prn (0.5-1mg PO, max 4mg in 24 hours)
Quetiapine (12.5mg od to 25mg bd)
Clozapine (12.5 - 50mg daily)
Cholinesterase inhibitors
Do not use anti dopaminergics!
339
Q

What acetylcholinesterase inhibitors are used in dementia?

A

Rivastigmine licensed for use in mild to moderate PD dementia
Tablets: 1.5mg bd (max 6mg bd)
Patch: 4.6mg/24 hours (max 9.5mg/24 hours)
Donepezil, Galantamine (not licensed for PD dementia)
NMDA receptor antagonists: Memantine

340
Q

Which drugs should be avoided in Parkinson’s?

A

Anything that blocks dopamine
Anti-emetics: Prochlorperazine, Metoclopramide, cyclizine
Antipsychotics: Chlorpromazine, promazine. Fluphenazine, perphenazine, prochlorperazine, trifluoperazine, Haloperidol

341
Q

What are the aims of treatment of stroke?

A

Reduce the ongoing neurological injury
Reduce mortality and long-term disability
Prevent complications
Prevent stroke recurrence

342
Q

When is tPA licensed for stroke treatment?

A

When given within 4.5 hours of symptom onset in 18-80 year olds with no evidence of haemorrhage
Stroke symptoms present at least 30 minutes
A clearly measurable deficit (NIHSS - national institute of health stroke scale)

343
Q

What should be given in acute stroke if thrombolysis is not an option?

A

Aspirin 300mg stat (PO, PR, NG)

344
Q

What are contraindications to thrombolysis for stroke?

A

Other life threatening illness
Haemorrhagic retinopathy
Oesophageal varices
Recent (within 10 days) traumatic external cardiac massage, puncture of a non-compressible vessel
Manifest or recent severe or dangerous bleeding
Recent major surgery or trauma
Neoplasm with increased bleeding risk
Severe liver disease
Recent ulcerative GI disease
Acute pancreatitis
Bacterial endocarditis, pericarditis
Abnormal clotting/haemorrhagic diathesis
Platelet count <100x109/l
CT evidence of haemorrhage
Glucose >22.2mmol/l or <2.8mmol/l
Pretreatment systolic BP >185 mmHg or diastolic BP >110 mmHg
Severe stroke assessed by NIHSS (>25) or by imaging
Unknown time of onset
Symptoms suggestive of subarachnoid haemorrhage, even if CT is normal

345
Q

What are relative contraindications or times when caution should be used in thrombolysis for stroke?

A

Pregnant
Minor symptoms e.g. NIHSS < 5
Significant symptoms may be present even with NIHSS 0-4 e.g. dysphasia
Symptoms rapidly improving, consider treatment if significant symptoms still present after 30 mins
On Warfarin/heparin /LMW heparin/other anticoagulants, INR should be 1.7 or less
NOAC: consider tPA if starting 24 hours after last dose of NOAC (12-24 hrs if Dabigatran provided APTT is 1.3 or less)
Seizure at stroke-onset (seizure per se is not a CI but make sure weakness is not due to post-seizure paralysis)
Age > 80 years, consider ‘biological’ age
Patient dependent prior to stroke, consider level of dependency
Prior stroke and concomitant diabetes, consider current diabetic control, time interval between previous and current stroke,
level of dependency prior to current stroke
Stroke within the last 3 months, 6-8 weeks if the initial stroke was minor
Arterial aneurysm, AV malformations: small, incidental cerebral aneurysms may be allowed

346
Q

What are complications of thrombolysis for stroke?

A

Hypotension (slow infusion down)
Nausea and vomiting
Stop tPA infusion if: Major systemic bleeding, Anaphylaxis, Urticaria, bronchospasm, angioedema, hypotension/shock, Suspected ICH
Neuro deterioration (GCS drop or rise >2 NIHSS points)
New headache
Sustained hypertension

347
Q

After considering thrombolysis for stroke, what is the next management?

A

If given thrombolysis: Repeat CT head at 24 hours, If no haemorrhage start Aspirin 300mg OD
If not thrombolysed and no haemorrhage: Start Aspirin 300mg OD
Continue Aspirin 300mg od for total 2 weeks (then clopidogrel 75mg /day thereafter)
If Aspirin cannot be given: Clopidogrel 300mg single dose on day 1 and then Clopidogrel 75mg OD thereafter
Avoid anticoagulation - even in AF, Consider if required 2 weeks after acute stroke

348
Q

How should blood pressure be managed in acute stroke?

A

Aim initially for BP of 160-180 / 90-105
Treat if BP > 220/120 or if diastolic > 140
Labetalol iv 2-10mg over 2-5 mins
GTN infusion: bolus 5mg iv, then 1-4mg/hour

349
Q

What do new guidelines say about when patients should be seen after a TIA?

A

All patients with suspected TIA should be seen in 24hrs IRRESPECTIVE of risk– Seen in 7 days if symptoms from over 1 wk ago
Previously used ABCD2 score to determine risk
High risk (4-7): seen within 24 hours
Crescendo: may need admission
Low risk (0-3): assess and investigate within 7 days

350
Q

What are the components of the ABCD2 score?

A
Age 60 or over
Blood pressure over 140/90
Clinical features: unilateral weakness (2), speech disturbance (1)
Duration: >60 mins (2), 10-59 mins (1)
Diabetes
351
Q

How should TIA be managed?

A

All patients with suspected TIA get aspirin 300mg at presentation unless contraindicated
All patients with proven TIA clopidogrel 300mg
Day 2 onwards: Clopidogrel 75 mg OD, High intensity statin therapy (eg atorvastatin 20-80mg daily)
All patients need carotid dopplers within 24 hrs (if significant stenosis use second mode of imaging that is non invasive to confirm)
Anticoagulation: If patient is in AF, start anticoagulation immediately if no contraindications (CT head first to exclude haemorrhage)
Blood pressure: Aim for secondary prevention target of < 130/80

352
Q

What are risk factors for stroke?

A

Non-modifiable: age, male, familial predisposition
Blood pressure: risk doubles for every 7.5 mmHg increase in diastolic BP
Cholesterol: increase with total cholesterol, LDL cholesterol and low HDL levels
Cigarette smoking: doubles risk of stroke death
AF: 4% annual risk (increase to 12% if previous TIA/stroke), 5 fold increase risk of stroke
Diabetes: 2-4 fold increase risk of stroke
Valvular heart disease: risk of 10-20% per yr
Carotid stenosis: risk is 2% per yr in asymptomatic stenosis of 75%, increase to 15% if recent event
Other: OCP, HRT, physical inactivity, obesity

353
Q

What are contraindications to the use of NOACs?

A

Presence of prosthetic heart valve (bioprosthetic and mechanical valves although edoxaban is approved with bioprosthetic valves after the first 3 months)
Renal impairmen
Concomitant use of prohibited medications including HIV protease
inhibitors, systemic azoles, dronedarone, rifampicin, carbamazepine, phenytoin
Liver disease eg enzymes > x2 upper limit of normal

354
Q

What are the components of the CHA2DS2VASC score?

A
Congestive heart failure
HTN
Aged 75 or more (2)
Diabetes
Stroke/TIA (2)
Vascular disease
Aged 65-74
Sex female
355
Q

What are the components of the has bled score?

A
HTN
Abnormal renal and liver function (1 point each)
Stroke
Bleeding
Labile INR 
Elderly
Drugs or alcohol (1 point each)
356
Q

How may a brain tumour present?

A

Space occupying lesion / raised intracranial pressure
Headache resistant to pain relief
Vomiting
Epilepsy
Altered state of consciousness
Frontal lobe: changed mood behavior reasoning disturbed speech
Temporal lobe: disturbed memory, language, reasoning, temporal
lobe epilepsy
Parietal lobe: aphasia, disturbed sensory or motor function poor spatial visual perception
Occipital lobe: disturbed vision and visual loss
Cerebellum: disturbed balance and gait

357
Q

What is the WHO grading system for CNS tumours?

A

Grade I tumors are slow-growing, nonmalignant, and associated with long-term survival, Low cellularity, No pleomorphism
Grade II tumors are relatively slow-growing but sometimes recur as higher grade tumors. They can be nonmalignant or malignant, Low to moderate cellularity, Mild pleomorphism
Grade III tumors are malignant and often recur as higher grade tumors, High cellularity, Infiltrative, Definite pleomorphism, mitoses
Grade IV tumors reproduce rapidly and are very aggressive malignant
tumors, Vascular proliferation, Tumour necrosis

358
Q

What is MEN1?

A

Pituitary adenoma
Pancreas tumours
Parathyroid hyperplasia

359
Q

What is tuberous sclerosis?

A

Multi-system disease
Benign tumours (hamartomas) in brain, heart (rhabdomyomas) kidney (angiofibroma) lung (lymphangioleiomyomatosis), skin (adenoma subaceum)
Mutations in tumour supressor genes TSC1 (Hamartin) TSC2(Tuberin)
CNS involvement: Cortical Tubers, Sub-ependymal nodules, Giant cell astrocytomas, Seizures, developmental delay, behavioural problems

360
Q

What is neurofibromatosis type1?

A
Autosomal dominant
Deletion in neurofibromin gene Chr 17q11.2
Negative regulator of RAS
Multiple schwannomas and neurofibromas
Peripheral nerves
Multiple musculoskeletal abnormalities
Café au-lait patches on the skin
Lisch nodules on the iris
Cognitive learning disability
361
Q

What is neurofibromatosis type2?

A

NFII merlin or schwannomin chr 22q11-13.1
Acoustic neuroma (vestibular neuroma), Cerebropontine angle
50% develop tumours in other cranial nerves and spinal cord
Skin tumours
cataracts

362
Q

What is carneys complex?

A

Myxoma of heart and skin
Hyperpigmentation of skin (lentiginosis)
Primary pigmented nodular adrenocortical disease (pituitary tumour)

363
Q

What is the different between a macro and micro pituitary adenoma?

A

10mm or more macro-adenomas, under 10mm microadenomas

364
Q

What are the 4 main types of glial cell?

A

Astrocytes, oligiodendrocytes, ependyma and microglial cells

365
Q

What is a craniopharygioma?

A

Arises in the pituitary stalk
Derived from Rathke’s pouch
Sqamous epithelial tumour
Locally invasive

366
Q

Which spinal level is affected to cause paraplegia?

A

T1-L5

367
Q

Which spinal level is affected to cause tetraplegia?

A

C1-C8

368
Q

What are red flags in headache?

A
Early Morning Headache
Vomiting with Headache
Vision Problems
Sudden Onset Headaches
Thunderclap Headache
Fever and rash, neck stiffness/photophobia
369
Q

What is management for tension headache?

A
Simple analgesics
Stress reduction
Acupuncture
Lifestyle changes: Reduce caffeine, cheese, red meat, weight loss, stay hydrated
? amitriptyline
370
Q

What is the management of migraine?

A

Lifestyle: avoid triggers, headache diary
Terminate: Sumitriptan, NSAID, paracetamol
Sickness: Metoclopramide, Prochlorperazine, domperidone
Prevention: Propranolol, topiramate, up to 10 sessions of acupuncture over 5-8 weeks if medication ineffective, riboflavin

371
Q

What are triggers for migraine?

A
Menstruation
Altered sleep
Stress
Food: chocolate, cheese, caffeine, alcohol
Strong smells
Bright light
Dehydration 
Missed meals
Jet lag
Strenuous exercise
372
Q

In which migraine patients should prevention medication be considered?

A

> 4 attacks per month
Producing disability lasting 3 days or more
Person at risk of medication overuse headache
Standard analgesia and triptans are contraindicated/ineffective

373
Q

What specific questions should you ask to diagnose GCA?

A
Headache?
Jaw claudication?
Scalp tenderness?
Visual disturbances?
Proximal limb muscle pain and tenderness?
374
Q

What clinical findings might you expect with temporal arteritis?

A

Non-pulsatile temporal artery
Tenderness over temporal artery
As it is a vasculitis need to examine whole peripheral vascular system

375
Q

How do you manage GCA?

A

Take blood for inflammatory markers: ESR
Start prednisolone 60mg daily oral
Counsel with regard to medication and side-effects
Start aspirin 75 mg daily (unless contra-indications)
Start gastroprotection with PPI in view of added risk of peptic ulceration with high-dose steroids and aspirin
Low-dose aspirin has been shown to decrease rate of visual loss and strokes in patients with GCA
Arrange temporal artery biopsy
Arrange review in next few days
Safety-net: if visual problems, go to A and E

376
Q

What are characteristics of a migraine headache?

A

Paroxysmal headaches, severe unilateral, although 30-40% bilateral
Premonitory phase in 20-60%
Aura
Photophobia, vomiting, nausea with marked headache but course highly variable
Resolution phase occurs as headache gradually fades
Feel tired, irritable, depressed and have difficulty concentrating

377
Q

What is a premonitory phase in migraine?

A

Different from an aura, occurs hours to days before headache
Feeling that a migraine is imminent
Depression, tiredness, difficulty concentrating, irritability, stiff neck and food cravings
Many different features can be present but they tend to be consistent for the individual

378
Q

What is a migraine aura?

A

Progressive, gradual onset over minutes, last five minutes to an hour and occur before headache
Visual disturbance starts in one eye and may spread. It may be homonymous. Is fully reversible
Sensory symptoms (paraesthesia or numbness) are unilateral and fully reversible. Numbness usually starts in hand and moves up arm before involving face, lips and tongue. Leg is sometimes affected. Numbness may follow paraesthesia. Sensory auras rarely occur alone and usually follow visual auras
Aura has no motor symptoms
Headache either begins before end of aura or within an hour of the end and has the same features as migraine without aura
One patient may at different times have migraine attacks with and without aura
Sometimes no headache may follow a typical aura - but always consider possibility of transient ischaemic attack (TIA) rather than migraine in these patients, particularly if the patient says the aura was different from their usual aura

379
Q

What are contraindications to use of triptans for migraine?

A

Uncontrolled hypertension
Coronary heart disease or cerebrovascular disease
Risk factors for coronary heart disease or cerebrovascular disease
Coronary vasospasm (Prinzmetal’s angina)

380
Q

Which migraine medications can be used in pregnancy?

A

Paracetamol

381
Q

What is a medication overuse headache?

A

Headache developing as a consequence of regular overuse of acute or symptomatic headache medication for over 3 months
Use of simple analgesics and NSAIDs on 15 days or more per month
Triptans, opioids and combination analgesics on 10 days or more per month

382
Q

What is the management of medication overuse headache?

A

Stop analgesics abruptly or
Wean down by increasing, by 1 day each week, number of
medication-free days
Opiates and codeine-based medication may need to be gradually reduced, as withdrawal symptoms can be severe

383
Q

In patients with total loss of consciousness, which features would warrant urgent referral for cardiovascular assessment?

A

An ECG abnormality
Heart failure (history or physical signs)
TLoC during exertion
Family history of sudden cardiac death in people aged younger than 40 years and/or an inherited cardiac condition
New or unexplained breathlessness
A heart murmur
Consider referring within 24 hours for cardiovascular assessment, as above, anyone aged older than 65 years who has experienced TLoC without prodromal symptoms

384
Q

Which patients with total loss of consciousness need referring for assessment of epilepsy?

A

A bitten tongue
Head-turning to one side during TLoC
No memory of abnormal behaviour that was witnessed before, during or after TLoC by someone else
Unusual posturing
Prolonged limb-jerking (note that brief seizure-like activity can often occur during uncomplicated faints)
Confusion following the event
Prodromal déjà vu, or jamais vu

385
Q

Which medications can cause tremor?

A

Atypical antipsychotics
Anti-nausea agents (metoclopramide, prochlorperazine, promethazine)
Calcium-channel blockers (flunarizine, cinnarizine)
Dopamine depletors (reserpine, tetrabenazine)
Antidepressants (SSRI, TCA, MAOI)
Mood stabilisers (lithium)
Antiepileptic drugs (valproic acid)
Cardiac drugs (amiodarone)
Immunosuppressants (ciclosporin, tacrolimus, corticosteroids)
Anti-asthma drugs (salbutamol, theophylline)
Stimulants (amphetamines)

386
Q

What investigations can be done for tremor?

A

Renal, liver, bone biochemistry
TFTs
May need MRI or CT brain
May need 24-hour urinary copper and serum caeruloplasmin if suspect Wilson’s disease

387
Q

What are causes of tremor?

A
Parkinson's disease 
Lewy body dementia 
Hypoglycaemia
Thyrotoxicosis
Alcohol withdrawal
Essential tremor 
Drug-induced
Uncommon: Multiple system atrophy, Progressive supra-nuclear palsy, Cortical basal degeneration, Toxin-induced, Phaeochromocytoma, Cerebellar tremor (MS, trauma, stroke) Fragile X tremor ataxia syndrome (FXTAS), Orthostatic tremor, Primary writing tremor, Neuropathic tremor, Wilson's disease, Rubral tremor (combined coarse rest and action tremor), Psychogenic tremor
388
Q

What is Todds paresis?

A

Transient weakness of hand, arm or leg after focal seizure activity within that limb

389
Q

Which tests are part of a confusion screen?

A
AMTS
FBC
U and Es
LFTs
Calcium
Glucose
TFTs
B12
Folate
390
Q

What are features of myasthenia gravis?

A
Muscle fatigability 
Extraocular muscles: diplopia
Proximal muscle weakness: face, neck, limb girdle
Ptosis
Dysphagia
391
Q

What are associations of myasthenia gravis?

A

Thymoma
Thymic hyperplasia
Autoimmune disorders: pernicious anaemia, autoimmune thyroid disease, rheumatoid, SLE

392
Q

How should myasthenia gravis be investigated?

A

Single fibre electromyography
CT thorax to exclude thymoma
CK (normal)
Autoantibodies to ACh receptor, muscle specific tyrosine kinase antibodies
Tensilon test: IV edrophonium reduces muscle weakness temporarily (risk of cardiac arrhythmia)

393
Q

What is the management of myasthenia gravis?

A

Long acting anticholinesterase: pyridostigmine
Immunosuppressants: prednisolone initially
Thymectomy
Myasthenic crisis: plasmapheresis, IV immunoglobulins

394
Q

Which drugs are associated with idiopathic intracranial HTN?

A

Isotretinoin
Tetracycline antibiotics
Hormonal contraceptives

395
Q

Which migraine auras would be considered atypical and may prompt further investigation?

A
Motor weakness
Double vision
Unilateral visual symptoms
Poor balance
Decreased consciousness
396
Q

What are features of multiple system atrophy?

A

Parkinsonism
Autonomic disturbance: atonic bladder, postural hypotension
Cerebellar signs

397
Q

What does the facial nerve supply?

A

Muscles of facial expression
Stapedius
Taste anterior 2/3 tongue
Parasympathetic to lacrimal and salivary glands

398
Q

What are causes of bilateral facial nerve palsy?

A

Sarcoidosis
Guillain barre syndrome
Polio
Lyme disease

399
Q

What are causes of unilateral facial nerve palsy?

A
Stroke (UMN)
Bell’s palsy
Ramsay hunt syndrome
Acoustic neuroma
Parotid tumour
HIV 
MS
Diabetes 
Sarcoidosis 
Guillain barre syndrome 
Polio
Lyme disease
400
Q

What is the difference between upper and lower motor neuron lesions of the facial nerve?

A

UMN: spares upper face
LMN: affects all facial muscles

401
Q

What are neurological causes of SIADH?

A
Surgical or traumatic damage to brain
Encephalitis/brain abscess
Brian tumour
Meningitis
Guillain barre 
Cerebrovascular accidents
Subdural haematoma
Tumour of 4th ventricle 
Neonatal hypoxia 
Hydrocephalus
402
Q

What is Gaucher’s disease?

A

Inherited autosomal recessive disorder of lipid metabolism due to beta glucosidase deficiency
Causes accumulation of glycolipids in phagocytic cells and cells of CNS
Features: hepatosplenomegaly, neuro dysfunction, bone erosions of long bones, pingueculae (orange wedge shaped deposits in subconjunctiva and yellow brown discolouration of skin in areas exposed to sun

403
Q

What is the difference between Guillain barre and miller fisher syndrome?

A

Guillain barre: paralysis without sensory loss, areflexia

Miller fisher: areflexia, ataxia, opthalmoplegia, no weakness

404
Q

What are type 1 and 2 Charcot Marie tooth?

A

Inherited motor and sensory neuropathy
Type 1: demyelinating, autosomal dominant
Type 2: axonal, can be dominant or recessive

405
Q

What abnormalities would you expect with superficial peroneal nerve damage?

A

Paraesthesia in central dorsum of foot and proximal toes except 5th
Weakness of eversion of foot

406
Q

What are chronic neurological sequelae from kernicterus?

A

Athetosis
Gaze disturbance
Hearing loss

407
Q

What is the world federation of neurological societies grading system for SAH?

A
Grade 1: GCS 15
Grade 2: GCS 13-14 no deficit
Grade 3: GCS 13-14 focal deficit 
Grade 4: GCS 7-12 
Grade 5: GCS <7
408
Q

Which part of the cerebellum is affected if there is truncal ataxia with minimal limb signs?

A

Cerebellar vermis

Hemispheres if limb signs and less truncal

409
Q

What are causes of Cerebellar syndrome?

A

MS
Stroke
Alcohol
Phenytoin

410
Q

What are differences between Cerebellar and vestibular nystagmus?

A

Cerebellar: fast towards lesion and worse towards affected side
Vestibular: fast away from lesion and worse looking away

411
Q

In a patient with upper motor neurone signs in the legs only, where is the lesion?

A

In spinal cord, above L1

412
Q

What is pyramidal weakness?

A

Flexors in arms stronger than extensors

Extensors in legs stronger than flexors

413
Q

What are differentials for a mixed picture of upper and lower motor neurone signs?

A

MND
Freidreichs ataxia
Subacute combined degeneration of the cord
Tabes dorsalis

414
Q

How can you examine for myotonia?

A

Thenar eminence tap, slow to relax

Grip of hands, difficult to release

415
Q

What is pronator drift a sign of?

A

UMN pyramidal lesion