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Neurology Flashcards

1
Q

Differentials for headache

A
  • Tension headaches
  • Migraines
  • Cluster headaches
  • Secondary headaches
  • Sinusitis
  • Giant cell arteritis
  • Glaucoma
  • Intracranial haemorrhage
  • Subarachnoid haemorrhage
  • Analgesic headache
  • Hormonal headache
  • Cervical spondylosis
  • Trigeminal neuralgia
  • Raised intracranial pressure (brain tumours)
  • Meningitis
  • Encephalitis
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2
Q

Red Flags for headaches

A
  • Fever, photophobia or neck stiffness  MENINGITIS OR ENCEPHALITIS
  • New neurological symptoms  HAEMORRHAGE, MALIGNANCY, STROKE
  • Dizziness  STROKE
  • Visual disturbance  TEMPORAL ARTERITIS OR GLAUCOMA
  • Sudden onset occipital headache  SUBARACHNOID HAEMORRHAGE
  • Worse on coughing or straining  RAISED INTRACRANIAL PRESSURE
  • Postural, worse on standing, lying or bending over  RAISED INTRACRANIAL PRESSURE
  • Severe enough to wake from sleep
  • Vomiting  RAISED INTRACRANIAL PRESSURE OR CO POISONING
  • History of trauma  INTRACRANIAL HAEMORRAGE
  • Pregnancy  PRE-ECLAMPSIA
  • Previous headache history + progression or change in character
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3
Q

Types of migraine

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (aura but no headache)
  • Hemiplegic migraine (mimic stroke)
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4
Q

Triggers of migraine

A
  • Chocolate
  • Hangovers, dehydration
  • Orgasms
  • Cheese
  • Oral contraceptives
  • Lie-ins (abnormal sleep patterns)
  • Alcohol
  • Tumult = loud noise, strong smells, bright lights
  • Exercise
  • Stress
  • Menstruation
  • Trauma
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5
Q

Stages of migraine

A
  1. Premonitory/prodromal stage = 3 days before
  2. Aura = up to 60 mins
  3. Headache = 4-72 hours
  4. Resolution
  5. Post-dromal or recovery
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6
Q

Presentation of migraine

A
  • Prodrome = yawning, cravings, mood/sleep changes
  • Headache lasting 4-72 hours
    o Moderate to severe intensity
    o Pounding or throbbing in nature
    o Usually unilateral but can be bilateral
  • Nausea and vomiting
  • Photophobia/phonophobia (sound sensitive)
  • Motion sensitivity
  • Visual or other aura lasting 15-30 mins
    o Sparks, lines, blurring in vision
    o Loss of different visual fields
    o Paraesthesiae spreading from fingers to face
  • Hemiplegic migraine
    o Typical migraine symptoms
    o Hemiplegia (unilateral weakness of limbs)
    o Ataxia
    o Speech = dysphasia or paraphasiae
    o Changes in consciousness
  • Papilloedema
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7
Q

Management of migraine

A
  • Dark quiet room and sleep
    1. Paracetamol or NSAIDs + oral triptan
    o S/E = Tingling, heat, tightness, heaviness, pressure
    o CI = Hx of IHD or cerebrovascular disease
  • Antiemetics – if vomiting (metoclopramide)
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8
Q

Prevention of migraines

A
  • Keep headache diary to identify triggers and avoid triggers
  • Propranolol (not in asthma)
  • Topiramate (not in pregnancy or women of child bearing age)
  • Amitriptyline
  • Botox
  • 10 sessions of Acupuncture over 5-10 wks
  • Supplementation with B2 (riboflavin)
  • NSAIDS/triptans (if associated with menstruation)
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9
Q

Risk factors for tension headache

A
  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger (skipping meals)
  • Eyestrain
  • Anxiety/Depression
  • Noise
  • Alcohol
  • Dehydration
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10
Q

Presentation of tension headache

A
  • Can be episodic (<15 days/month) or chronic (>15 days/month for at least 3 months)
  • Bilateral pressing/tight non-pulsatile headache
    o Mild/moderate intensity
    o Headaches can last from 30 mins to 7 days
    o Comes on and resolves gradually
  • Scalp muscle tenderness
  • Pressure behind eyes
  • No visual changes
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11
Q

Management of tension headache

A
  • Lifestyle
    o Reassurance and lifestyle advice
    o Stress relief and relaxation techniques
    o Hot towels to local area
  • Medication
    o Basic analgesia  paracetamol, ibuprofen, aspirin
    o TCA  amitriptyline
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12
Q

Risk factors for cluster headache

A

Smoking

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13
Q

Triggers of cluster headache

A
  • Alcohol
  • Strong smells
  • Exercise
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14
Q

Presentation of cluster headaches

A
  • Episodic = clusters last 4-12 wks and followed by pain-free periods of months-yrs
  • Chronic = attacks for more than 1 yr without remission
  • Sudden excruciating stabbing unilateral pain around one eye, temple or forehead
    o Rises in crescendo over mins and last 15 mins to 3 hrs
    o Once or twice a day (usually same time)
    o Often nocturnal/early morning = wakes patient from sleep
  • Vomiting
  • Restlessness or agitation
  • Red swollen, watering eye with lid swelling
  • Facial flushing/sweating
  • Rhinorrhoea (nasal discharge)
  • Miosis (excessive pupil constriction)
  • Ptosis (eyelid dropping)
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15
Q

Management of cluster headaches

A
  • SC sumatriptan
  • High flow O2 for 15 mins via non-breathable mask
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16
Q

Prophylaxis of cluster headaches

A
  • 1st line = CCB (verapamil)
  • Avoid alcohol
  • Prednisolone (short course for 2-3 wks)
  • Lithium
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17
Q

What is giant cell arteritis

A

Chronic vasculitis characterised by granulomatous inflammation in walls of medium and large arteries

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18
Q

Presentation of GCA

A
  • New-rapid onset headache (temporal) <1m
  • Temporal artery abnormality
    o Tenderness on palpation of temporal artery
    o Thickening
    o Nodularity
    o Red overlying skin
    o Pulsation (reduced or absent)
  • Visual disturbances
    o Loss of vision
    o Diplopia
    o Changes to colour vision
    o Fundoscopy  pallor and oedema of optic disc, cotton wool patches, small haemorrhages in retina
  • Scalp tenderness (brushing hair)
  • Scalp necrosis
  • Intermittent jaw claudication
  • Systemic features  Low grade fever, Fatigue, Anorexia, Weight loss, Depression, Night sweats
  • Features of PMR  proximal muscle pain, morning stiffness, tenderness, aching
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19
Q

Investigations for GCA

A
  • Raised inflammatory markers  ESR >50
  • Temporal artery biopsy  skip lesions
  • Creatine kinase and EMG normal
  • Vision testing
    o Anterior ischaemic optic neuropathy
    o Temporary visual loss
    o Diplopia
    o Swollen pale disc and blurred margins
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20
Q

Management of GCA

A
  • MEDICAL EMERGENCY
  • Urgent high-dose Glucocorticoids = 40-60mg oral prednisolone per day for 1-2 yrs
    o Given before temporal artery biopsy
    o No visual loss  prednisolone
    o If visual loss give IV methylprednisolone
    o Should be dramatic response
  • Urgent ophthalmology review = Visual damage often irreversible
  • Bone protections with bisphosphonates
  • Low dose aspirin
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21
Q

Complications of GCA

A
  • Loss of vision
  • Aortic aneurysm
  • Aortic dissection
  • Large artery stenosis
  • Aortic regurgitation
  • CVD = MI, HF, stroke, peripheral arterial disease
  • Scalp necrosis, peripheral neuropathy, depression, confusion, encephalopathy, deafness
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22
Q

Management of analgesia overuse headache

A
  • Withdrawal of analgesia
    o Immediately for paracetamol, NSAIDs or triptans
    o Gradually for opiates
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23
Q

Presentation of trigeminal neuralgia

A
  • 90% unilateral, 10% bilateral
  • Intense electricity-like shooting facial pain, comes on spontaneously
  • Lasts between few secs to hrs
  • Attacks worsen over time
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24
Q

Management of trigeminal neuralgia

A
  • Carbamazepine
  • Surgery to decompress or intentionally damage nerve
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25
Q

Causes of raised intracranial pressure

A
  • Brain tumours
  • Intracranial haemorrhage
  • Idiopathic intracranial hypertension
  • Abscesses or infection
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26
Q

Presentation of raised intracranial pressure

A
  • Constant headache (often nocturnal)
    o Worse on waking, coughing, straining or bending forward
  • Vomiting
  • Altered mental state
  • Visual field defects
  • Seizures
  • Unilateral ptosis
  • 3rd and 6th nerve palsies
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27
Q

Fundoscopy findings in papilloedema

A

o Blurring of optic disc margin
o Elevated optic disc
o Loss of venous pulsation
o Engorged retinal veins
o Haemorrhages around optic disc
o Paton’s lines (creases in retina around optic disc)

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28
Q

Risk factors for idiopathic intracranial hypertension

A
  • Obesity
  • Pregnancy
  • Drugs = COCP, steroids, tetracyclines (lymecycline), Vit A, lithium
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29
Q

Presentation of idiopathic intracranial hypertension

A
  • Headache
  • Blurred vision
  • Papilloedema
  • Enlarged blind spot
  • 6th nerve palsy
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30
Q

Management of idiopathic intracranial hypertension

A
  • Weight loss
  • Diuretics = acetazolamide
  • Topiramate
  • Repeated LP
  • Surgery
    o Optic nerve sheath decompression and fenestration
    o Lumboperitoneal or ventriculoperitoneal shunt
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31
Q

Types of brain tumour

A
  • Meningiomas (benign)
  • Gliomas  Astrocytoma, Oligodendroglioma, Ependymoma
  • Glioblastomas (highly malignant)
  • Pituitary tumours
  • Acoustic neuroma (schwann cells)
  • Secondary metastases (lung, breast, renal cell carcinoma, melanoma)
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32
Q

Presentation of brain tumours

A
  • Asymptomatic when small
  • Features of ICP  headache, vomiting, seizures, 3rd and 6th nerve palsies, visual field defects, papilloedema, altered mental state, unilateral ptosis
  • Fatigue
  • Hearing loss, tinnitus, balance problems (acoustic neuroma)
  • Temporal lobe  dysphasia, amnesia
  • Frontal lobe  hemiparesis, personality change, Broca’s dysphasia, lack of initiative, unable to plan tasks
  • Parietal lobe  hemisensory loss, reduction in 2-point discrimination, dysphasia, astereognosis (unable to recognise object from touch alone)
  • Occipital lobe contralateral visual defects
  • Cerebellum  dysdiadochokinesis (impaired rapidly alternative movement), ataxia, slurred speech (dysarthria), hypotonia, intention tremor, nystagmus, gait abnormality (DASHING)
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33
Q

Management of brain tumours

A
  • Palliative care
  • Surgery = remove mass depending on grade
  • Chemotherapy (6 weeks post-op)
  • Radiotherapy
  • Oral dexamethasone = steroid to improve brain performance
  • Oral carbamazepine = anticonvulsant
  • Pituitary tumours
    o Trans-sphenoidal surgery
    o Radiotherapy
    o Bromocriptine (block prolactin-secreting tumours)
    o Somatostatin analogues (block GH secreting tumours)
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34
Q

Causes of brain abscess

A
  • Extension of sepsis from middle ear or sinuses
  • Trauma or surgery to scalp
  • Penetrating head injuries
  • Embolic events from endocarditis
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35
Q

Presentation of brain abscess

A
  • Raised ICP
  • Headache = dull, persistent
  • Fever
  • Focal neurology = e.g. oculomotor nerve palsy
  • Nausea
  • Papilloedema
  • Seizures
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36
Q

Management of brain abscess

A
  • NEUROLOGICAL EMERGENCY
  • Surgery  Craniotomy and abscess cavity debrided
  • IV Abx  IV 3rd generation cephalosporin and metronidazole
  • ICP management  Dexamethasone
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37
Q

Risk factors for subarachnoid haemorrhage

A
  • Berry aneurysms
    o Hypertension
    o Connective tissue disorders = Marfan or Ehlers-Danlos syndrome
    o Autosomal dominant polycystic kidney disease
    o Coarctation of aorta
  • Smoking
  • Excessive alcohol consumption
  • Cocaine use
  • Sickle cell anaemia
  • Neurofibromatosis
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38
Q

Presentation of SAH

A
  • Thunderclap headache during strenuous activity
    o Severe occipital pain peaking within 1-5 mins
  • Meningism  Neck stiffness, Photophobia
  • Nausea and vomiting
  • Speech changes, weakness, seizures
  • Depressed level of consciousness, coma
  • Kernig’s sign = unable to extend patients leg at knee when thigh is flexed
  • Brudzinski’s sign = when patients neck is flexed by doctor, patient will flex hips and knees
  • Papilloedema
  • Vision loss or diplopia (double vision)
  • Fixed dilated pupils = signs of CN3 palsy caused by pressure on CN3 seen in posterior communicating artery aneurysm
  • Marked increase in BP
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39
Q

Investigations for SAH

A
  • Non-contrast CT head = ‘star-shaped lesion’
  • If CT head within 6 hrs of Sx onset and normal consider alternative diagnosis
  • If CT head done >6hrs after Sx onset and normal  do a LP
  • Lumbar puncture at >12 hrs
    o Xanthochromia (yellow CSF caused by bilirubin)
    o Red cell count raised
    o Normal or raised opening pressure
  • Angiography = locate source of bleeding
  • ECG  ST elevation
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40
Q

Management of SAH

A
  • Refer to neurosurgery
    o Endovascular coiling or clipping = treat aneurysms
  • Nimodipine (CCB) = prevent vasospasm
  • Intubation and ventilation
  • IV fluids and maintain BP
  • Lumbar puncture or insertion of shunt = hydrocephalus
  • Antiepileptic medications
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41
Q

Complications of SAH

A
  • Very high mortality and morbidity
  • Rebleeding
  • Cerebral ischaemia
  • Hydrocephalus
  • Hyponatraemia due to SIADH
  • Vasospasm
  • Seizures
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42
Q

Risk factors for SDH

A
  • Elderly
  • Traumatic head injury
  • Cerebral atrophy/increasing age
  • Alcoholism
  • Dementia
  • Anticoagulation
  • Physical abuse of infant
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43
Q

Cause of SDH

A

Rupture of bridging veins in outermost meningeal layer

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44
Q

Presentation of SDH

A
  • Raised ICP symptoms
  • Headache
  • Sleepiness
  • Vomiting and nausea
  • Personality change
  • Unsteadiness
  • Seizures occasionally
  • Raised BP
  • Hemiparesis or sensory loss
  • Stupor, coma
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45
Q

Investigations for SDH

A
  • Non-contrast CT head <48 hrs
    o Crescent shape on 1 hemisphere and not limited by cranial sutures
    o Dark/hypodense = chronic
    o Bright hyperdense = acute
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46
Q

Management of SDH

A
  • ABCDE then refer to neurosurgeons
  • Burr hole craniotomy and clot evacuation
  • IV mannitol to reduce ICP
  • Phenytoin (if seizures)
  • Address cause of trauma = Fall due to cataract, arrhythmia, abuse etc
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47
Q

Complications of SDH

A

Tectorial herniation and coning

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48
Q

Cause of extradural haemorrhage

A

Traumatic head injury leading to laceration of middle meningeal artery

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49
Q

Presentation of EDH

A
  • Brief post-traumatic loss of consciousness or initial drowsiness
  • Severe headache
  • Nausea and vomiting
  • Confusion
  • Seizures
  • Rapid rise in ICP
  • Hemiparesis (weakness of half side of body) with brisk reflexes
  • Ipsilateral pupil dilates
  • Breathing becomes deep and irregular = brainstem compression
  • Decreased GCS
  • Coning = Brain herniates through foramen magnum
  • Bradycardia and raised BP
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50
Q

Investigations of EDH

A
  • CT head = biconvex shape and limited by cranial sutures
  • Skull XR = fracture lines crossing course of middle meningeal artery
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51
Q

Management of EDH

A
  • ABCDE
  • Refer to neurosurgery
    o Burr hole craniotomy
    o clot evacuation +/- ligation of bleeding vessel
  • IV mannitol for increased ICP
  • Maintain intubation and ventilation
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52
Q

Causes of cerebellar disorder

A
  • Stroke or TIA
  • Hydrocephalus
  • Posterior fossa tumours or abscess
  • Thiamine deficiency
  • Vitamin E deficiency
  • Gluten sensitivity
  • Meningo-encephalitis or intracranial abscess
  • Acute or chronic viral infections (HIV)
  • Parasitic infections
  • Creutzfeldt-Jakob disease
  • Alcohol
  • Carbon monoxide poisoning
  • Drugs = barbiturates, phenytoin, piperazine, antineoplastic drugs
  • Drug overdose
  • Trauma
  • Multiple sclerosis
  • Lung, gynae, breast cancer or Hodgkin’s lymphoma
  • Friedreich’s ataxia
  • Cerebral oedema of chronic hypoxia
  • Inherited metabolic disorders
  • Cerebral palsy
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53
Q

What is cerebral palsy

A

Group of permanent movement and posture disorders that limit activity due to non-progressive lesion of motor pathways in developing brain

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54
Q

Prenatal factors for cerebral palsy

A

o Multiple gestation
o Chorioamnionitis
o Maternal respiratory tract or genito-urinary infection treated in hospital
o Thyroid disease, iodine deficiency, TORCH
o Maternal thrombotic disorders (factor V Leiden mutations)
o Teratogen exposure (warfarin)
o Fetal genetic and metabolic disorders
o Fetal brain malformations
o Placental abruption

55
Q

Perinatal factors for cerebral palsy

A

o Preterm birth
o Low birth weight
o Respiratory distress
o Birth asphyxia
o Intraventricular haemorrhage
o Hyperbilirubinaemia
o Neonatal sepsis
o Neonatal encephalopathy

56
Q

Postnatal factors for cerebral palsy

A

o Head injuries (<3y)
o Meningitis
o Intraventricular haemorrhage
o Hypoglycaemia
o Hydrocephalus

57
Q

Presentation of cerebral palsy

A
  • Low APGAR score at birth
  • Posturing
    o Abnormal limb/trunk posture
    o Persistent toe-walking
  • Oropharyngeal problems
    o Tongue thrusts, grimacing, swallowing difficulties
    o Feeding difficulties
  • Strabismus
  • Tone
    o Abnormal tone early infancy (increased or decreased)
    o Asymmetric hand function before 12m
    o Abnormal gait
    o Difficulty in changing nappies (stiff limbs)
    o Delayed motor milestones  not sitting by 8m, not walking by 18m
    o Late head control, rolling and crawling
  • Evolutional response
    o Persistent primitive reflexes (palmar grasp, rooting)
    o Failure to develop equilibrium and protective responses
  • Reflexes
    o Deep tendon reflexes increased
    o Plantar reflexes up going
  • Diarrhoea
  • Learning difficulties
  • Epilepsy
  • Squints
  • Hearing impairment
58
Q

Management of cerebral palsy

A
  • MDT coordinated care
  • Minimise complications and comorbidities
  • Treat spasticity
    o Oral diazepam
    o Oral and intrathecal Baclofen
    o Botox
    o Anticonvulsants
  • Analgesia
  • Surgical treatment
    o Repair of scoliosis, tendon lengthening, osteotomy
    o Selective dorsal rhizotomy
59
Q

Complications and comorbidities of cerebral palsy

A
  • Feeding difficulties
  • Sialorrhoea/drooling
  • Aspiration, recurrent chest infection
  • Vomiting, regurgitation, GORD
  • Osteopenia, osteoporosis
  • Constipation
  • Incontinence
  • Visual impairment
  • Hearing impairment
  • Epilepsy
  • Learning disability
  • Communication difficulties
  • Behavioural difficulties
  • Mental/psychological health problems, neurodevelopmental disorders
  • Pain
  • Sleep disturbance
  • Impaired social interaction and participation
  • Reduced quality of life
  • Reduced life expectancy
60
Q

Causes of seizures

A
  • Abnormal blood vessels in brain
  • Alzheimer’s/dementia
  • Use of drugs = cocaine
  • Alcohol withdrawal
  • Head injury years before onset
  • Cerebrovascular disease = cerebral infraction or haemorrhage
  • CNS infection = meningitis or encephalitis
  • Stroke/brain tumour
61
Q

Generalised tonic clonic seizures

A

o Loss of consciousness
o Muscle tensing and muscle jerking
o Tongue biting, incontinence, groaning, irregular breathing
o Prolonged post-ictal = confused, drowsy, irritable, depressed

62
Q

Management of generalised tonic clonic seizures

A

o (male) = sodium valproate
o (female child-bearing age) = lamotrigine or carbamazepine

63
Q

Focal seizures

A

o Affect hearing, speech, memory and emotions
o Hallucinations
o Memory flashbacks/ Déjà vu
o Automatisms  lip smacking, grabbing, plucking

64
Q

Management of focal seizures

A

o carbamazepine or lamotrigine
o sodium valproate or levetiracetam

65
Q

Absence seizures

A

o Children (most stop as they get older)
o Blank, stares into space then abruptly returns to normal
o Unaware of surroundings and won’t respond
o Lasts 10-20s

66
Q

Management of absence seizures

A

o ethosuximide
o sodium valproate

67
Q

Atonic seizures

A

o Brief lapses in muscle tone
o Last under 3 mins
o Begin in childhood
o Lennox-Gastaut syndrome

68
Q

Management of atonic seizures

A

o sodium valproate
o lamotrigine

69
Q

Myoclonic seizures

A

o Sudden brief muscle contractions (sudden ‘jump’)
o Remains awake
o Juvenile myoclonic epilepsy

70
Q

Management of myoclonic seizures

A

o sodium valproate
o lamotrigine, levetiracetam, topiramate

71
Q

Infantile spasms/West syndrome

A

o Starts around 6m
o Clusters of full body spasms
o Poor prognosis

72
Q

Management of infantile spasms

A

1st line = prednisolone or vigabatrin

73
Q

Other features of epileptic seizures

A
  • Jacksonian march = seizure marches up/down motor homunculus starting in face or thumb
  • Post-ictal Todd’s palsy = paralysis of limbs involved in seizure for several hours
  • Frontal lobe  head/leg movements, posturing, post-ictal weakness, Jacksonian march
  • Parietal lobe  paraesthesia
  • Occipital lobe  floaters/flashes
74
Q

Advice for epileptic patients

A

o Inform DVLA = cannot drive until seizure free for 6m post seizure or 1 year with established epilepsy
o Avoid swimming/bathing alone, dangerous sports
o Breastfeeding considered safe with most AED
o Lamotrigine most suitable if wanting to get pregnant

75
Q

Differences between epilepsy and syncope

A

Tongue biting
Head turning
Muscle pain
Loss of consciousness
Cyanosis
Post-ictal symptoms

76
Q

Side effects of sodium valproate

A

Teratogenic (contraception advice and avoided in women/girls unless alternative)
Liver damage and hepatitis
Hair loss
Tremor
Increased appetite and weight gain
Ataxia
Thrombocytopenia

77
Q

Side effects of carbamazepine

A

Agranulocytosis
Aplastic anaemia
Induces P450 system so many drug interactions (e.g. Warfarin)
Dizziness and ataxia
Drowsiness
Inappropriate ADH secretion

78
Q

Side effects of phenytoin

A

Folate and vitamin D deficiency
Megaloblastic anaemia
Osteomalacia
Peripheral neuropathy
Lymphadenopathy

79
Q

Side effects of lamotrigine

A

Stevens-Johnson syndrome or DRESS syndrome (life threatening skin rashes)
Leukopenia

80
Q

Presentation of non-epileptic attack disorders

A
  • Seizures lasting over 2 mins
  • Gradual onset
  • Fluctuating course
  • Violent thrashing movements
  • Side-to-side head movement
  • Asynchronous movements
  • Eyes closed
  • Recall for period of unresponsiveness
  • Pelvic thrusting
  • Family member with epilepsy
  • History of mental health conditions and/or trauma
  • Crying after seizure
  • Doesn’t occur when alone
81
Q

Causes of facial nerve palsy

A

UMN lesions
* Unilateral = cerebrovascular accidents, tumours
* Bilateral = pseudobulbar palsies, MND
LMN lesions
* Bell’s palsy
* Ramsay-Hunt syndrome
* Infection = otitis media, HIV, lyme disease
* Systemic = DM, sarcoidosis, leukaemia, MS, GBS
* Tumours = acoustic neuroma, parotid tumours, cholesteatomas
* Trauma = surgery, base of skull fractures

82
Q

Difference between UMN and LMN facial nerve palsy

A

UMN lesion = forehead will be spared
LMN lesion = forehead will not be spared

83
Q

MAangement of bell’s palsy

A

Majority recover over several weeks (up to 12m)
Within 72 hrs of symptoms  Prednisolone
* 50mg for 10 days
* 60mg for 5 days followed by 5 day reducing regime of 10mg a day
Eye care
* Lubricating eye drops
* Tape eye closed at bed time
* Ophthalmology review
If no improvement after 3 wks refer urgently to ENT
Refer to plastic surgery if long-standing weakness for surgical decompression

84
Q

Presentation of horner’s syndrome

A

Partial ptosis = upper eyelid drooping
Miosis = pupillary constriction
Hemifacial anhidrosis = absence of sweating
Facial flushing
Orbital pain/headache

85
Q

Presentation of Parkinson’s disease

A
  • Gradual onset of symptoms
  • Resting Tremor
    o Often asymmetrical
    o Usually most obvious in hands (pill rolling tremor)
    o Improved by voluntary movements and made worse by anxiety/distracted
    o Using other hand exaggerates tremor
    o Issue with repetitive hand movements with worsening in rhythm the longer attempted
    o Not present in sleep
  • Rigidity = extrapyramidal lesion
    o Cogwheel rigidity
    o Increased tone in limbs and trunk
    o Spasticity where resistance falls away as movement continues
    o Resistance to passive movement of joint (tension give way in small increments)
    o Can cause pain and problems with turning in bed
  • Bradykinesia
    o Slow to initiate movement and slow, low-amplitude excursions in repetitive actions
    o Reduced blink rate
    o Monotonous hypophonic speech (indistinct and flat)
    o Difficulty with fine movements
    o Micrographia = smaller writing
    o Expressionless face (facial masking)
  • Gait
    o Reduced asymmetrical arm swing
    o Stooped posture
    o Shuffling gait (small steps, dragging foot)
    o Difficulty initiating movement (standing to walking) and turning
    o Poor balance and postural instability
    o Forward tilt
  • Other
    o Depression
    o Sleep disturbance and insomnia
    o Loss of sense of smell
    o Cognitive impairment and memory problems
    o Drooling of saliva and swallowing difficulty = late feature
86
Q

Management of Parkinson’s disease

A
  • Physiotherapy and Physical activity
  • Oral levodopa along with peripheral decarboxylase inhibitor (Co-careldopa/ co-beneldopa)
    o Delay use with other drugs first
    o Becomes less effective over time
  • Dopamine agonists = Oral ropinirole/ oral pergolide
    o Avoid bromocriptine/cabergoline
  • Monoamine oxidase B inhibitors = oral selegiline or oral rasagiline
  • Catechol-O-methyl transferase inhibitors = Oral entacapone/ tolcapone
  • SSRIs for depression = Oral citalopram
  • Anti-psychotics = Oral quetiapine
  • Deep brain stimulation = Help those who are partly-dopamine responsive
  • Surgical ablation of overactive basal ganglia circuits
87
Q

Differences between Parkinson’s and benign essential tremor

A

Parkinson’s
Asymmetrical
4-6Hz
Worse at rest
Improves with intentional movement
Other parkinson’s features
No change with alcohol

BET
Symmetrical
5-8Hz
Improves at rest
Worse with intentional movement
No other Parkinson’s features
Improves with alcohol

88
Q

Side effects of levodopa

A

Dyskinesias (abnormal movements associated with excessive motor activity)
e.g. dystonia = excessive muscle contraction leade to abnormal postures/ exaggerated movement
e.g. chorea = abnormal involuntary movements
e.g. athetosis = involuntary twisting or writhing movements (fingers, hands, feet)
Reduced efficacy over time even if dose increased
On-dyskinesias = hyperkinetic, choreiform movement whenever drugs work
Off-dyskinesias = fixed, painful dystonic posturing
Freezing = unpredictable loss of mobility

89
Q

Causes of essential tremor

A
  • Physiological
  • Post-traumatic
  • Medication
  • MS
  • Parkinsonism
  • Metabolic derangement
  • Wilson’s disease
  • Cerebellar disease
  • Basal ganglia lesions
  • Dystonias
  • Vitamin deficiency (B1)
90
Q

Management of essential tremor

A
  • May not require treatment (mild)
  • Intermittent treatment (mild-moderate)
  • Treatment options
    o Propranolol
    o Primidone
    o Others = topiramate, atenolol, alprazolam, clonazepam, gabapentin
  • Head tremor = botox
  • Deep brain stimulation
  • Thalamotomy
  • High-intensity focused US with MRI guidance
91
Q

Presentation of Huntington’s disease

A
  • Psychiatric problems (begins first)
    o Cognitive, psychiatric, mood problems
    o Behavioural change = Aggression, addictive behaviour, apathy and self-neglect
    o Depression/anxiety
  • Chorea
    o Relentlessly progressive, jerky, explosive, rigidity involuntary movements = ceases when sleeping
    o May begin as general restlessness, unintentionally initiated movements and lack of coordination
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
  • Seizures
  • Eye movement disorders
  • Dementia = Impaired cognitive abilities and memory
92
Q

Management of Huntington’s disease

A
  • Counselling to patient and family = Genetic counselling to any children of patients
  • SALT
  • Advanced directives and End of life care planning
  • Symptomatic management
    o Antipsychotics (olanzapine)
    o Benzodiazepines (diazepam)
    o Sulpiride = depresses nerve function
    o Tetrabenazine = dopamine depleting agent
    o Antidepressants (SSRIs) = seroxate
    o Antipsychotic mediation (Neuroleptics) = haloperidol
    o Treat aggression = Risperidone
93
Q

Presentation of normal pressure hydrocephalus

A
  • Gait abnormality (WOBBLY)
  • Urinary incontinence (WET)
  • Cognitive impairment (WACKY)
    o Memory loss
    o Inattention
    o Inertia
    o Bradyphrenia (slowness of thought)
  • Dizziness
  • Spasticity
  • Sudden ‘freezing’
  • Pyramidal tract signs
  • Brisk reflexes
94
Q

Management of normal pressure hydrocephalus

A
  • CSF shunt (ventriculoperitoneal)
  • Carbonic anhydrase inhibitors (acetazolamide)
  • Repeated LP
95
Q

Complications of CSF shunt

A
  • Shunt occlusion
  • Catheter breakage
  • CSF hypotensive headaches
  • Cerebral infarct
  • Haemorrhage
  • Infection
  • Seizures
96
Q

Causes of stroke

A
  • Ischaemia
    o Thrombus formation or embolus
    o Atherosclerosis
    o Large artery stenosis
    o Shock
    o Vasculitis
    o Hypoperfusion = sudden drop in BP
    o Hyperviscosity = polycythaemia and sickle cell
  • Haemorrhage
    o Trauma
    o Aneurysm rupture
    o Anticoagulation
    o Thrombolysis
    o Carotid artery dissection
    o Subarachnoid haemorrhage
97
Q

Classifications of stroke

A
  • Oxford stroke (Bamford) classification
  • Total anterior circulation infarcts = middle and anterior cerebral arteries
  • Partial anterior circulation infarcts = smaller arteries of anterior circulation
  • Lacunar infarcts = arteries around internal capsule, thalamus and basal ganglia
98
Q

Presentaiton of anterior cerebral artery stroke

A

o Contralateral hemiparesis
o Sensory disturbances
o Lower extremity > upper
o Gait apraxia = loss of normal function of lower limbs
o Truncal ataxia = can’t sit/stand unsupported and tend to fall backwards
o Incontinence
o Akinetic mutism = decrease in spontaneous speech, stuporous state

99
Q

Presentation of middle cerebral artery stroke

A

o Contralateral arm and leg weakness
o Sensory loss
o Contralateral homonymous hemianopia
o Aphasia = inability to understand speech
o Dysphasia = deficiency in speech generation
o Facial droop

100
Q

Presentation of posterior cerebral artery stroke

A

o Contralateral homonymous hemianopia with macular sparing
o Cortical blindness
o Visual agnosia = can see but not interpret visual information
o Prosopagnosia = cannot see faces
o Colour naming and discriminate problems
o Unilateral headache

101
Q

Weber’s syndrome

A

o Ipsilateral CNIII palsy
o Contralateral weakness of upper and lower extremity

102
Q

Posterior inferior cerebellar artery stroke

A

o Ipsilateral facial pain and temperature loss
o Contralateral limb/torso pain and temperature loss
o Ataxia
o Nystagmus

103
Q

Anterior inferior cerebellar artery stroke

A

Lateral pontine syndrome
Ipsilateral facial paralysis and deafness

104
Q

Retinal artery stroke

A

Amaurosis fumax

105
Q

Basilar artery stroke

A

‘locked in’ syndrome

106
Q

Lacunar stroke

A

o Unilateral weakness of face and arm, arm and leg or all 3
o Pure sensory loss
o Ataxic hemiparesis = cerebellar and motor symptoms

107
Q

Emergency diagnosis of stroke

A
  • ROSIER tool
  • Stroke likely if score above 0
108
Q

Investigations for stroke

A
  • Urgent non-contrast CT head/ diffusion weighted MRI before treatment = exclude haemorrhage
  • Pulse, BP, ECG = look for AF
  • Blood glucose = exclude hypoglycaemia
  • Specialist imaging
    o Establish vascular territory affected
    o Diffusion-weighted MRI (GS)
    o Non-contrast CT alternative
    o Carotid USS (carotid stenosis)
    o Endarterectomy (remove plaques or carotid stenting)
109
Q

Management of ischaemic stroke

A

o ABCDE = Hydration and oxygen if needed
o Aspirin 300mg (after CT) and continue for 2 weeks
o Thrombolysis with alteplase (within 4.5 hrs after excluding intracranial haemorrhage)
o Thrombectomy if occlusion is confirmed on imaging depending on location and time (not after 24 hrs)
o Clopidogrel 24 hrs after thrombolysis
o Monitoring for post thrombolysis complications (repeat CT)
o Stroke rehab

110
Q

Management of haemorrhagic stroke

A

o Frequent GCS monitoring
o Antiplatelets contraindicated
o Any anticoagulants should be reversed (Warfarin  beriplex and vit K)
o Control hypertension
o Manual decompression of raised ICP
o Diuretic = Mannitol

111
Q

SEcondary prevention of stroke

A
  • Lifelong platelet treatment = aspirin and dipyridamole/clopidogrel daily
    o Give PPI cover for aspirin (omeprazole)
  • Treat modifiable risk factors
    o Cholesterol treatment = simvastatin (not started immediately)
    o AF treatment = warfarin/ new oral anticoagulants (apixaban)
    o Blood pressure treatment = ACE-I (ramipril)
112
Q

Management of TIA

A
  • Immediate 300mg aspirin unless
    o Patient has bleeding disorder or taking anticoagulant
    o Already taking low dose aspirin
    o Aspirin contraindicated
  • Urgent review by specialist within 24 hrs
  • Secondary prevention
    o Clopidogrel
    o Aspirin + dipyridamole
    o Atorvastatin
  • Cannot drive for minimum 4 week
113
Q

What is myasthenia gravis

A

Autoimmune disease against nicotinic acetylcholine receptors in neuromuscular junction

114
Q

Exacerbating factors of myasthenia gravis

A
  • Penicillamine
  • Quindine, procainamide
  • Beta-blockers
  • Lithium
  • Phenytoin
  • Abx = gentamicin, macrolides, quinolones, tetracyclines
  • Pregnancy
  • Hypokalaemia
  • Infection
  • Change of climate
  • Emotion
  • Exercise
115
Q

Associations of myasthenia gravis

A
  • Thymomas
  • Autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
  • Thymic hyperplasia
116
Q

Presentation of myasthenia gravis

A
  • Muscle weakness and fatigability
    o Worse with muscle use, at end of day, in pregnancy, hypokalaemia, infection, emotion, drugs (opiates, BB, gentamicin)
    o Improves with rest, in morning
    o Affect proximal muscles and small muscles of head and neck
  • Extraocular muscle weakness  Prolonged upward gazing exacerbate diplopia
  • Eyelid weakness (repeated blinking) causing ptosis
  • Weakness in facial movements
  • Difficult with swallowing
  • Fatigue in jaw when chewing
  • Slurred speech
  • Repeated abduction of one arm 20 times
117
Q

Investigations for myasthenia gravis

A
  • Autoantibodies: Acetylcholine receptor antibodies (85%), Muscle-specific kinase antibodies
  • Single fibres electromyography
  • CT/MRI of thymus gland
  • Edrophonium/tensilon test = IV edrophonium chloride temporarily relieves weakness
  • Nerve conduction study
  • Ptosis improves by >2mm after ice application to shut lid for >2mins
  • Test FVC
  • Check for thymectomy scar
118
Q

Management of myasthenia gravis

A
  • Reversible acetylcholinesterase inhibitors  Pyridostigmine 1st line
  • Immunosuppression (prednisolone or azathioprine)
  • Monoclonal antibodies (rituximab)
  • Bone protection, PPI
  • Thymectomy
119
Q

Side effects of acetylcholinesterase inhibitors

A

increased salivation, lacrimation, sweats, vomiting, miosis, diarrhoea

120
Q

Complications of myasthenic gravis

A
  • Myasthenic crisis = weakness of respiratory muscles
    o Acute worsening of symptoms
    o Triggered by another illness (respiratory tract infection)
    o Can lead to respiratory failure
    o Plasma exchange and IV immunoglobulin
    o Non-invasive Ventilation with BIPAP or full intubation and ventilation
121
Q

Presentation of cauda equina

A
  • Low back pain
  • Bilateral sciatica
  • Reduced sensation/ pins and needles in perinanal area
  • Decreased anal tone
  • Urinary/bowel dysfunction
  • Erectile dysfunction
  • Variable leg weakness is flaccid and areflexic (LMN)
  • Saddle anaesthesia
122
Q

Presentation of motor neurone disease

A
  • Gait  Stumbling, spastic, tripping over
  • Cramps
  • Wrist and foot drop
  • Insidious, progressive weakness of muscles throughout body affecting limbs, trunk, face and speech
  • Increased fatigue when exercising
  • Clumsiness, dropping things
  • Slurred speech
  • Dysarthria, dysphagia, nasal regurgitation of fluids and choking
  • Jaw jerk is normal/absent
  • Speech is quiet, hoarse or nasal
  • Weak grip and shoulder abduction
123
Q

LMN signs

A

o Muscle wasting
o Reduced tone
o Reduced reflexes
o Split hand sign = Thumb side of hand seems adrift due to excessive wasting around it
o Flaccid, fasciculating tongue

124
Q

UMN signs

A

o Increased tone or spasticity
o Brisk reflexes
o Upgoing plantar responses

125
Q

Management of MND

A
  • Riluzole = slow progression of disease and extend survival
  • Oral propantheline/amitriptyline = prevents drooling
  • Treat dysphagia = blend food, NG tube, percutaneous catheter gastrostomy
  • Oral baclofen = spasms
  • Analgesia
  • Non-invasive ventilation if respiratory failure
  • Advanced directives and End of life care planning
126
Q

Presentation of multiple sclerosis

A
  • Symptoms pattern
    o Usually progress over more than 24 hrs
    o At first symptoms last days to wks then improve
    o Uhthoff’s phenomena = Symptoms may worsen with heat/exercise
    o Improve during pregnancy and postpartum
  • Charcot’s neurological triad  Dysarthria, Nystagmus, Intention tremor
  • Sensory features
    o Dysaesthesia
    o pins and needles
    o decreased vibration sense
    o trigeminal neuralgia
    o Lhermitte’s sign = sudden sensation like electric shock travels down spine into limbs worse when bending head to chest
  • Motor  Spastic weakness and myelitis
  • Neuro  Cognitive problems, Depression
  • Autonomic  urinary urgency, frequency, incontinence, erectile dysfunction
  • Cerebellar  loss of proprioception, positional vertigo, ataxia
  • Dysphagia
  • Constipation
  • Nausea and vomiting
  • Unilateral optic neuritis
  • Eye movement abnormalities = Diplopia, hemianopia, pupil defects
  • 6th cranial nerve palsy = internuclear ophthalmoplegia and conjugate lateral gaze disorder
  • Horner’s syndrome
  • Bell’s palsy
  • Limb paralysis
127
Q

Investigations of multiple sclerosis

A
  • Diagnosis requires 2+ attacks affecting different parts of CNS (separated by time and space)
  • MRI brain and spinal cord with contrast
    o periventricular lesions
    o white matter abnormalities
    o multiple scattered plaques
    o High signal T2 lesions
    o Dawson fingers = hyperintense lesions perpendicular to corpus callosum
  • Lumbar puncture  oligoclonal IgG bands which are not in serum (not specific)
  • Increased intrathecal synthesis of IgG
128
Q

Management of multiple sclerosis

A
  • Acute relapse
    1. Oral methylprednisolone for 5 days
    2. IV methylprednisolone 3-5 days when failed or severe
  • Remission = dimethyl fumarate
  • Treatment with DMARDs and biological therapy
  • Symptomatic Tx
    o Exercise
    o Amitriptyline/gabapentin = neuropathic pain
    o Antidepressants (SSRIs) = depression
    o Tolterodine or catheterisation = urge incontinence
    o Baclofen, physio = spasticity
    o Reduce stress
    o Vitamin D supplements
    o Botulinium toxin infections = tremor
    o Amantadine, CBT, exercise = fatigue
129
Q

Causes of peripheral neuropathy

A
  • Predominantly motor loss
    o Guillain-Barre syndrome
    o Porphyria
    o Lead poisoning
    o Hereditary sensorimotor neuropathies (Charot-Marie- Tooth)
    o Chronic inflammatory demyelinating polyneuropathy
    o Diphtheria
  • Predominately sensory loss
    o Diabetes
    o Uraemia
    o Leprosy
    o Vit B12 deficiency
    o Amyloidosis
    o Alcoholic neuropathy = Secondary to both direct toxic effects and reduced absorption of B vits
  • Sensory Sx before Motor
    o Vitamin B12 deficiency
    o Subacute combined degeneration of spinal cord
    o Dorsal column usually affected first prior to distal paraesthesia
130
Q

Presentation of Guillain-Barre syndrome

A
  • History of respiratory or GI infections 1-3 wks prior to onset
  • Back and limb pain
    o Symptoms typically start at feet and progress upward
    o Symptoms peak 2-4 wks
    o Recovery period last months to yrs
  • Symmetrical ascending muscle weakness
    o Starts 1-3 wks post infection
    o Advance quickly, affecting all limbs at once
    o Can lead to paralysis
    o Proximal muscles more affected = trunk, respiratory and cranial nerves (CN7)
  • Reduced/absent reflexes
  • Peripheral loss of sensation or neuropathic pain
  • May progress to cranial nerves and cause facial nerve weakness
    o Diplopia
    o Bilateral facial nerve palsy
    o Oropharyngeal weakness
    o Papilloedema
  • Autonomic features  Sweating, raised pulse, BP changes, arrhythmias, urinary retention, diarrhoea
131
Q

Investigations for GBS

A
  • Clinical diagnosis using Brighton criteria
  • Nerve conduction studies (reduced signal through nerves)
    o Decreased motor nerve conduction velocity
    o Prolonged distal motor latency
    o Increased F wave latency
  • LP (L4)  CSF has raised protein but normal WCC and glucose
  • Spirometry = Monitor FVC if respiratory involvement
132
Q

Management of GBS

A
  • Admit to hospital
  • IV immunoglobulin for 5 days
    o Contraindicated in patients with IgA deficiency
  • Plasma exchange (alternative to IV Ig)
133
Q

Presentation of common peroneal nerve lesion

A
  • Foot drop
  • Weakness of foot dorsiflexion
  • Weakness of foot eversion
  • Weakness of extensor hallucis longus
  • Sensory loss of dorsum of foot and lower lateral part of leg
  • Wasting of anterior tibial and peroneal muscles

Finals (23 decks)

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