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Phase 3a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Syncope

A

Loss of consciousness due to transient global cerebral hypoperfusion

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2
Q

What is the commonest cause of transient loss of consciousness?

A

Syncope

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3
Q

What is the most common cause of syncope?

A

Vasovagal (faint)

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4
Q

What are some triggers of vasovagals?

A

Sudden surprise/fear
Pain
Sight of blood
Prolonged standing
Venesection

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5
Q

What is the mechanism of vasovagals?

A

Vagus nerve receives a strong stimulus, which stimulates the parasympathetic nervous system, resulting in reflex bradycardia +/- peripheral vasodilation, causing the BP to drop and hypoperfusion of the brain

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6
Q

What are some causes of syncope?

A

Vasovagal
Carotid sinus hypersensitivity
Hypoglycaemia
Anaemia
Hypovolaemia, e.g. haemorrhage, ruptured aneurysm, dehydration
Cardiac
Infection
Anaphylaxis
Epileptic seizures
Postural hypotension
Functional
Hyperventilation
Micturition syncope
Cough syncope

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7
Q

What is carotid sinus hypersensitivity?

A

Mild external pressure on carotid bodies in the neck (shaving, neck turning, tight collar) induces a reflex response resulting in transient loss of consciousness

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8
Q

What are some cardiac causes of syncope?

A

Arrhythmias
Valvular heart disease
Hypertrophic cardiomyopathy
Pulmonary embolus

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9
Q

What is postural hypotension?

A

Drop in BP of more than 20mmHg or reflex tachycardia of more than 20bpm when a person goes from lying down or sitting to standing, due to delay in constriction of veins of the leg resulting in blood pools and less venous return to the heart

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10
Q

What are some medications that can increase your risk of syncope?

A

Block vasoconstriction: calcium channel blockers, beta blockers, alpha blockers, nitrates
Affect volume status: diuretics
Prolong the QT interval: antipsychotics, antiemetics

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11
Q

What is the clinical manifestation of syncope?

A

Brief prodrome: dizziness, lightheadedness, nausea, sweating, hot or clammy, blurry vision, pallor, feeling of heaviness, headache
Sudden loss of consciousness and fall to the ground, with unconsciousness lasting for a few to 30 seconds
Rapid recovery

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12
Q

Associated symptoms of syncope

A

Palpitations
Sweats
Pallor
Chest pain
Dyspnoea

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13
Q

Investigations for syncope

A

Bloods
* U&E (arrhythmia, seizure)
* FBC (anaemia)
* Mg and Ca
* Glucose (DM)
* ABG (hyperventilation)

Cardiovascular examination (palpitations, arrhythmias)
* 12-lead ECG +/- 24 hour ECG (arrhythmias, heart block, prolonged QT interval)
* Echocardiogram (structural heart disease

Neurological examination
* CT/MRI brain
* EEG

Lying and standing BP (postural hypotension)
* Tilt-table test

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14
Q

What are some differences between syncope and seizures?

A

Triggers
Prodrome
Duration
Convulsions
Colour
Lateral tongue biting
Recovery

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15
Q

What is the management of vasovagals?

A
  • Avoid triggers
  • Early recognition of prodromal symptoms in order to sit/lie down or use physical counter-pressure manoeuvres (leg and knee crossing, squatting, hand gripping and arm tensing)
  • Lifestyle modifications: adequate fluid intake and regular meals
  • Review medications
  • Fludrocortisone
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16
Q

How to manage postural hypotension

A
  • Sit rather than stand where possible
  • Sit first when moving from lying to standing
  • Eat frequent small meals and adequate fluid intake
  • Head-up sleeping
  • Compression garments (abdominal binders or support stockings)
  • Early recognition of prodromal symptoms in order to sit/lie down or use physical counter-pressure manoeuvres (leg and knee crossing, squatting, hand gripping and arm tensing)
  • Review medications
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17
Q

What is brain death?

A

Irreversible loss of capacity for consciousness and to breathe due to cessation of brainstem function

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18
Q

Clinical manifestation of brain death

A

Apnoeic coma (unresponsive on a ventilator, with no spontaneous respiratory efforts)

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19
Q

What is the management for brain death?

A
  • Stop mechanical venilation and other life-supporting measures
  • Retrieval of organs while heart is still beating for transplantation (if organ donor)
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20
Q

How is brain death examined?

A

2 senior doctors
* Absent reflexes - oculocephalic, light, corneal, vestibulo-occular on caloric testing, gag or cough
* Fixed, unresponsive pupils
* No motor response within the cranial nerve territory to painful stimuli applied centrally or peripherally
* Absent spontaneous respiration

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21
Q

What must be diagnosed in order to announce brain death?

A

Irremediable structural brain damage due to a disorder that can cause brainstem death, e.g. head injury, intracranial haemorrhage

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22
Q

What reversible causes of coma must be excluded before announcing brain death?

A
  • Sedative drugs, poisoning or neuromuscular blocking agents
  • Hypothermia
  • Metabolic disturbances
  • Endocrine disturbances
  • Abnormal plasma electrolytes
  • Abnormal acid-base balance
  • Abnormal blood glucose levels
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23
Q

Define essential tremor

A

Fine tremor during voluntary muscle contraction that typically involves the hands and is brought about by anti-gravity positions, e.g. outstretched hands

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24
Q

What are the characteristics of an essential tremor?

A
  • Fine tremor (6-12Hz)
  • Symmetrical
  • More prominent with voluntary movement or voluntarily maintained in a certain position (drinking from a cup)
  • Improved by alcohol
  • Absent during sleep
  • Progressive disorder that worsens over time
  • Most notable in hands but can affect other areas
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25
Q

What are risk factors for an essential tremor?

A

Older
Family history (autosomal dominant)

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26
Q

How is essential tremor diagnosed?

A

Clinically: upper limb action tremor +/- tremor in other sites for over 3 years with no other neurological features

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27
Q

What investigation rules out other potential diagnoses of essential tremor?

A

MRI/dopamine transporter CT scan

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28
Q

What is the management of an essential tremor?

A
  • Stop triggers
  • Propranolol (beta blocker)
  • Primidone (antiepileptic)
    Only if causing problems!
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29
Q

Motor neurone disease

A

Progressive, degenerative and eventually fatal disease where the motor neurones stop functioning

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30
Q

What are the different types of motor neurone disease and which is the most common?

A
  • Amyotrophic lateral sclerosis: UMN + LMN
  • Progressive bulbar palsy: LMN of cranial nerves 9, 10, 11 and 12
  • Progressive muscular atrophy: LMN
  • Primary lateral sclerosis: UMN
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31
Q

What are the risk factors for motor neurone disease?

A
  • Advancing age (60)
  • Male
  • Family history
  • Smoking
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32
Q

What genetics are associated with amyotrophic lateral sclerosis?

A
  • Mutations in superoxide dismutase (SOD1)
  • Excess hexanucleotide repeats (GGGGCC)
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33
Q

What is the classic presentation of motor neurone disease?

A

Insidious, progressive weakness of muscles throughout the body, affecting limbs, trunk, face and speech, often first noticed in the upper limbs
* Hand weakness, with loss of dexterity and dropping things
* Wrist drop
* Foot drop, with difficulties with balance, particularly when running, leading to tripping over

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34
Q

What are signs of LMNs being affected in MND?

A
  • Muscle wasting
  • Reduced tone
  • Fasciculation, especially the tongue
  • Reduced reflexes
  • Muscle cramps
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35
Q

What are signs of UMNs being affects in MND?

A
  • Increased tone or spasticity
  • Brisk reflexes
  • Upgoing plantar reflex
  • Jaw clenching
  • Exaggerated jaw jerk
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36
Q

What are signs of progressive bulbar palsy?

A
  • Dysarthria
  • Dysphasia
  • Nasal regurgitation of fluids and choking
  • Absent jaw jerk reflex
  • Flaccid and fasciculating tongue
  • Jaw spasms
  • Cognitive problems
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37
Q

How is motor neurone disease diagnosed?

A

Clinically
* Definite: LMN + UMN signs in 3 region
* Probable: LMN + UMN signs in 2 regions
* Probable: LMN + UMN signs in 1 region or UMN sign in more than 1 region + electromyography showing acute denervation in more than 2 limbs
* Possible: LMN + UMN signs in 1 region
* Suspected: LMN or UMN sign in 1 or more regions

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38
Q

What investigations can rule out other potential diagnoses of MND?

A
  • MRI spine (cervical cord compression, myelopathy)
  • Lumbar puncture (inflammatory causes)
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39
Q

What is the management for MND?

A
  • Oral riluzole
  • If reduced FVC: non-invasive ventilation to support breathing at night
  • Antispasmodics
  • Antimuscarinics (saliva)
  • Analgesia
  • PEG tube
  • Therapy: SALT, physio
  • Advanced care plan and end of life care planning
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40
Q

What are complications of MND?

A
  • Aspiration pneumonia
  • Respiratory failure
  • Nocturnal respiratory insufficiency - nocturnal awakening, unrefreshed sleep, morning headaches
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41
Q

What is the prognosis for MND?

A

Most die within 3 years of onset of symptoms
80% die within 5 years

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42
Q

What is an acoustic neuroma?

A

Benign slow-growing tumour of Schwann cells surrounding the auditory nerve that innervates the inner ear

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43
Q

What are risk factors for acoustic neuroma?

A
  • Neurofibromatosis type 2 (suspect in bilateral acoustic neuromas)
  • Exposure to low-dose radiation in childhood
  • Noise
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44
Q

Where do acoustic neuromas occur?

A

Cerebellopontine angle (between cerebellum and pons) on the auditory nerve

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45
Q

What is the presentation of acoustic neuroma?

A

Gradual onset of:
* Unilateral sensorineural hearing loss
* Unilateral tinnitus
* Dizziness or imbalance
* A sensation of fullness in the ear

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46
Q

What is used to diagnose acoustic neuroma?

A

Brain imaging (CT/MRI)

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47
Q

How is acoustic neuroma classified?

A

Koos classification

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48
Q

What is the management of acoustic neuroma?

A

ENT
* Conservative monitoring if no symptoms
* Surgery to remove the tumour (suboccipital retrosigmoid approach, translabyrinthine approach, middle fossa approach)
* Radiotherapy to reduce growth

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49
Q

What are complications of acoustic neuroma?

A
  • Cranial nerve palsies
  • Hydrocephalus
  • Cerebellar dysfunction
  • Intracranial tumour (of cerebellopontine angle)
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50
Q

What are complications of acoustic neuroma treatment?

A
  • Vestibulocochlear nerve injury, with permanent hearing loss or dizziness
  • Facial nerve injury, with facial weakness
  • Persistent headaches
  • Bleeding
  • Infection
  • CSF leaks
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51
Q

Neurofibromatosis

A

Genetic condition causing benign nerve tumours (neuromas)

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52
Q

What is the cause of neurofibromatosis?

A
  • Type 1 (more common): autosomal dominant mutation on chromosome 17, which codes for a protein called neurofibromin 1, a tumour suppressor protein
  • Type 2: autosomal dominant mutation on chromosome 22, which codes for a protein called merlin, a tumour suppressor protein important in Schwann cells
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53
Q

What are the diagnostic criteria for neurofibromatosis type 1?

A
  • Cafe-au-lait spots
  • Relative with NF1
  • Axillary or inguinal freckling
  • Bony dysplasia - bowing of long bone or sphenoid wing dysplasia
  • Iris hamartomas
  • Neurofibromas (2 or more skin-coloured raised nodules or papules with a smooth regular surface, or a single larger irregular complex neurofibroma containing multiple cell types)
  • Glioma of the optic pathway
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54
Q

How is neurofibromatosis managed?

A

Surgical removal if symptoms develop

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55
Q

What are complications of neurofibromatosis type 1?

A
  • Migraines
  • Epilepsy
  • Renal artery stenosis (HTN)
  • Learning disability
  • ADHD
  • Scoliosis of the spine
  • Vision loss (optic nerve glioma)
  • Malignant peripheral nerve sheath tumours
  • GI stromal tumour
  • Brain tumour
  • Spinal cord tumour
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56
Q

What is chronic fatigue syndrome?

A

Persistent disabling fatigue lasting more than 6 months

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57
Q

What are the criteria for chronic fatigue syndrome?

A
  • Lasting more than 6 months
  • Affects mental and physical function
  • Present over 50% of the time
  • Plus 4 more of: myalgia, polyarthralgia, decreased memory, unrefreshing sleep, fatigue after exertion which lasts over 24 hours, persistent sore throat or tender cervical/axillary lymph nodes
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58
Q

What are some predisposing risk factors for chronic fatigue syndrome?

A
  • Perfectionist and introspective personality traits
  • Childhood trauma
  • Similar illnesses in first-degree relatives
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59
Q

What are some precipitating risk factors for chronic fatigue syndrome?

A
  • Infections (infectious mononucleosis, viral hepatitis)
  • Traumatic events, especially accidents
  • Life events that precipitate changed behaviour, e.g. taking time off sick
  • Incidents where they believe others are responsible
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60
Q

Risk factors for perpetuating chronic fatigue syndrome?

A
  • Inactivity with consequent physiological adaption
  • Avoidant behaviour
  • Maladaptive illness beliefs
  • Excessive dietary restrictions
  • Stimulant drugs, e.g. caffeine
  • Sleep disturbance
  • Mood disorders
  • Somatization disorder
  • Unresolved anger or guilt
  • Disputed compensation claim
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61
Q

What is the management of chronic fatigue syndrome?

A
  • Explanation of ill health, including diagnosis and causes, and education about management
  • Stop drugs, e.g. caffeine and analgesics
  • CBT to challenge unhelpful beliefs and change coping strategies
  • Graded exercise therapies to reduce inactivity and improve fitness
  • Antidepressants for mood disorders and sleep disturbance
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62
Q

Wernicke’s encephalopathy

A

Acute encephalopathy characterised by a triad of confusion, ataxia and oculomotor dysfunction

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63
Q

What causes Wernicke’s encephalopathy?

A

Thiamine (vitamin B1) deficiency

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64
Q

What are risk factors for Wernicke’s encephalopathy?

A
  • Chronic alcoholism (thiamine poorly absorbed in presence of alcohol)
  • Poor dietary intake - anorexia nervosa, prolonged fasting, starvation
  • Systemic malignancy
  • End-stage renal failure
  • GI disease and malabsorption
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65
Q

What are the clinical manifestations of Wernicke’s encephalopathy?

A
  • Confusion
  • Oculomotor dysfunction - nystagmus, conjugate gaze palsies, lateral rectus palsy
  • Ataxia
  • Hypothermia
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66
Q

What criteria is used for Wernicke’s encephalopathy?

A

Cane criteria: presence of more than 1 of the following criteria in patients with chronic alcoholism
* Dietary deficiency
* Oculomotor abnormalities
* Cerebellar dysfunction
* Altered mental status or mild memory impairment

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67
Q

What is the management for Wernicke’s encephalopathy?

A
  • Stabilisation and resuscitation
  • IV thiamine 250mg
  • Magnesium
  • Folic acid
  • Multivitamins
  • Abstain from alcohol
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68
Q

What are complications of Wernicke’s encephalopathy?

A
  • Coma and death
  • Inability to walk
  • Deficits in learning and memory
  • Korsakoff’s syndrome
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69
Q

What is Korsakoff’s syndrome?

A

Late neuropsychiatric manifestation of Wernicke’s encephalopathy with chronic amnesic syndrome characterised by defects in both anterograde and retrograde memory

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70
Q

What are characteristics of Korsakoff’s syndrome?

A
  • Memory impairment
  • Behavioural changes
  • Confabulation (stories made up to fill gaps in memory)
  • Disorientation to time
  • Poor insight
  • Global cognitive dysfunction
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71
Q

What is the management of Korsakoff’s syndrome?

A
  • IV thiamine
  • Consider magnesium, potassium and/or phosphate replacement

Often irreversible requiring care

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72
Q

Coma

A

Unrousable unresponsiveness

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73
Q

A coma is a person with a GCS score less than or equal to what?

A

8

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74
Q

What does consciousness depend on?

A
  • Arousal (level of consciousness) - ascending reticular activating system projecting from brainstem to thalamus
  • Content of consciousness - cerebral cortex
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75
Q

Causes of coma

A
  • Drug overdose - alcohol, sedatives
  • CO poisoning
  • Traumatic brain injury
  • Hypoglycaemia
  • Hepatic encephalopathy
  • Respiratory failure with CO2 retention
  • Metabolic acidosis
  • Infections - encephalitis, meningitis, cerebral malaria
  • Subarachnoid haemorrhage
  • Brainstem neoplasm
  • Wernick-Korsakoff syndrome
  • Brain tumour
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76
Q

Initial examinations for coma

A
  • ABCDE
  • Vital signs
  • GCS
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77
Q

Parameters for GCS score

A
  • Eye opening - spontaneous (4), to speech (3), to pain (2), no response (1)
  • Motor response - obeys (6), localises (5), withdraws (4), flexion (3), extension (2), no response (1)
  • Verbal response - orientated (5), confused conversation (4), inappropriate words (3), incomprehensible sounds (2), no response (1)
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78
Q

What system examinations would you complete for someone in a coma?

A
  • General - signs of trauma, stigmata of other illnesses, skin, meningism
  • Cardiovascular
  • Respiratory
  • Abdominal (and rectal?)
  • Neurological
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79
Q

Neurological aspects of examining someone in a coma

A
  • Papilloedema and subhyaloid retinal haemorrhage
  • Pupils size and reaction to light
  • Eye movements and position - lack of vestibulo-ocular reflex (deep coma), slow side-to-side eye movements (light or deep coma)
  • Corneal and gag/cough reflex
  • Lateralisation of pathology - asymmetry of response to visual threat, drooping or dribbling on one side, unilateral flaccidity or spasticity, asymmetrical response to painful stimuli or tendon reflexes and plantar responses
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80
Q

Investigations for coma

A
  • Blood glucose
  • Drug screen - alcohol, salicylates, urine toxicology (benzodiazepines, narcotics, amfetamines)
  • U&E
  • CT brain
  • Lumbar puncture after risk assessment (!intracranial mass lesion!)
  • EEG
  • Calcium
  • LFT
  • TFT
  • Cortisol
  • ABG
  • Cerebral malaria and porphyria
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81
Q

Locked-in syndrome

A

Complete paralysis, except vertical eye movements/blinking in ventral pontine infarction (fully aware but unable to communicate)

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82
Q

Immediate management of coma

A
  • Consider intubation if GCS <8
  • Support circulation if required with IV fluids
  • Oxygen
  • Protect cervical spine unless trauma known not to be the cause
  • Treat cause - glucose for hypoglycaemia, buccal midazolam for seizure, IV cefotaxime for fever and meningism, aciclovir for encephalitis, IV naloxone for opiate intoxication, IV flumazenil for benzodiazpine intoxication, IV thiamine for Wernicke’s encephalopathy, artemether/quinine for malaria
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83
Q

Long-term management of coma

A
  • Turn to avoid pressure ulcers
  • Oral hygiene - mouthwashes, suction
  • Eye care - lid taping, irrigation
  • NG or IV fluids
  • Feeding via a fine bore-NG tube or PEG
  • Catheterisation and rectal evacuation when essential
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84
Q

Causes of Horner’s syndrome

A
  • Space-occupying lesion
  • MS
  • Cervical cord trauma
  • Stroke
  • Pancoast tumour
  • Cervical rib
  • Brachial plexus injury
  • Carotid artery dissection
  • Cavernous sinus pathology
  • Neck mass
  • Following thyroid/laryngeal/carotid surgery
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85
Q

Horner’s syndrome is caused by a lesion along which pathway?

A

Oculosympathetic

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86
Q

Classic triad of Horner’s syndrome

A

Ipsilateral
* Miosis (small pupil)
* Ptosis (drooping eyelid)
* Anhidrosis (lack of sweat)

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87
Q

How is Horner’s syndrome diagnosed?

A

Clinically

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88
Q

What tests confirm Horner’s syndrome?

A
  • Cocaine drops (block reuptake of noradrenaline leading to activation of pupillary dilator and subsequent dilatation)
  • Apraclonidine (pupil dilates due to alpha-1 receptor denervation supersensitivity)
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89
Q

Investigations for cause of Horner’s syndrome

A
  • CT angiography (carotid artery dissection)
  • MRI spine (spinal cord lesions)
  • MRI head (cavernous sinus)
  • CT chest (pancoast tumour)
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90
Q

How to localise where the lesion is in Horner’s syndrome

A

Hydroxyamphetamine eye drops (stimulate release of noradrenaline, enabling differentiation between first or second order lesions (pupillary dilatation) and third order lesions (no effect))

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91
Q

Management of acute painful Horner’s syndrome

A

Urgent assessment for carotid dissection, with urgent neuroimaging and discussion with a hyperacute stroke unit (HASU)

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92
Q

What is raised intracranial pressure?

A

Increase in volume of cranium
>15mmHg

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93
Q

Causes of raised intracranial pressure

A
  • Head injury
  • Haemorrhage
  • Brain tumour
  • Infection - meningitis, encephalitis, brain abscess
  • Hydrocephalus
  • Cerebral oedema
  • Status epilepticus
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94
Q

What is Cushing’s reflex?

A

Nervous system response to raised intracranial pressure, resulting in Cushing’s triad
1. Bradycardia
2. Irregular respirations
3. Widened pulse pressure (large difference between systolic and diastolic BP)

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95
Q

Pathophysiology of Cushing’s reflex

A
  • Initial increase in systemic BP and heart rate (decreased cerebral perfusion causes brain ischaemia which activates the sympathetic NS)
  • Heart rate decreases (carotid and aortic baroreceptors detect increased BP and activates the parasympathetic NS)
  • Irregular respirations followed by periods where breathing ceases completely (as pressure in the brain continues to rise, brainstem dysfunctions)
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96
Q

Presentation of raised intracranial pressure

A
  • Headache, worse on coughing and learning forward
  • Vomiting
  • Altered GCS - drowsiness, irritability, coma
  • Constriction and then dilatation of pupils
  • Blurred vision and peripheral visual field loss
  • Papilloedema
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97
Q

Investigations for raised intracranial pressure

A
  • CT head
  • Lumbar puncture if safe (measure opening pressure)
  • Bloods - U&E, FBC, LFT, glucose, serum osmolality, clotting, blood culture
  • Toxicology screen
  • Chest x-ray (infection)
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98
Q

Management of raised intracranial pressure

A
  • ABC
  • Correct hypotension (MAP > 90mmHg) and treat seizures
  • Elevate head of the bed to 35
  • If intubated, hyperventilate (cerebral vasoconstriction)
  • IV mannitol (osmotic diuretic)
  • Corticosteroids (methylprednisolone) if oedema surrounding tumour
  • Consider sedation (propofol), anti-epileptics and therapeutic hypothermia
  • Restrict fluid to < 1.5L / day
  • Monitor neuro-obs and ICP
  • Treat cause and exacerbating factors (e.g. hyperglycaemia and hyponatraemia)
  • Decompressive craniotomy or burrhole
  • CSF drainage
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99
Q

Complications of raised intracranial pressure

A
  • Herniation (brain tissue shifts to opposite side or down towards brainstem)
  • Infarction of brain tissue
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100
Q

What is multiple sclerosis?

A

Progressive autoimmune condition causing demyelination of oligodendrocytes of the CNS

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101
Q

What is the commonest cause of chronic neurological disability in young adults in the UK?

A

MS

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102
Q

Pathophysiology of MS

A

Immune system attacks and destroys the myelin sheath of oligodendrocytes of the CNS
* Myelin-reactive T lymphocytes enter brain though disruption in BBB and activated by myelin
* Activated T lymphocytes: change BBB so it expresses more receptors allowing immune cell infiltration and releases cytokines that recruit more immune cells (B lymphocytes, macrophages and microglia) and directly damage myelin
* B lymphocytes make antibodies and macrhages use these antibodies to attack and destroy myelin
* MS plaques form (T and B lymphocytes and macrophages)

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103
Q

Why do symptoms resolve in early MS?

A

Regulatory T lymphocytes inhibit type 4 hypersensitivity reaction (release of cytokines by T lymphocytes and recruitment of immune cells) allowing remyelination

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104
Q

Why do symptoms change over time in MS?

A

Lesions vary in location over time

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105
Q

Why are symptoms permanent in later stages of MS?

A

Remyelination is incomplete

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106
Q

If someone with MS presents with optic neuritis, where is the lesion?

A

Optic nerve and often others throughout the CNS, most of which are not causing symptoms

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107
Q

What are the different courses of MS?

A
  • Clinically isolated syndrome
  • Relapse-remitting MS
  • Secondary progressive MS
  • Primary progressive MS
  • Progressive relapsing MS
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108
Q

Which is the most common course of MS?

A

Relapse-remitting
Episodes of disease and neurological symptoms followed by recovery, tending to occur in different areas with each episode

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109
Q

What is the difference between secondary progressive and primary progressive MS?

A

Primary progressive worsens from point of diagnosis without relapses and remissions
Secondary progressive starts as relapse-remitting, but progressively worsens

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110
Q

What is progressive relapsing MS?

A

One constant attack but bout superimposed, during which disability increases even faster

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111
Q

Risk factors for MS

A
  • 20-40
  • Female
  • White
  • Family history
  • Viral infections (EBV)
  • Low vitamin D
  • Smoking
  • Obesity
  • Other autoimmune diseases
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112
Q

Uhthoff’s phenomenon

A

In MS, symptoms worsen with heat, e.g. hot bath

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113
Q

Presentation of MS

A
  • Optic neuritis
  • Abnormal eye movements
  • Focal weakness
  • Focal sensory loss
  • Cerebellar dysfunction
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114
Q

Symptoms of optic neuritis in MS

A
  • Reduced vision in one eye, developing over hours to days
  • Central scrotoma (enlarged central blind spot, pale optic disc)
  • Impaired colour vision (greying, particularly of reds)
  • Blurring
  • Relative afferent pupillary defect (constricts more when shining light in contralateral eye)
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115
Q

Symptoms of eye movement abnormalities in MS

A
  • Double vision
  • Oscillopsia (environment moving and unable to create stable image)
  • Internuclear ophthalmoplegia (INO; slowed adduction)
  • Conjugate lateral gaze disorder
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116
Q

If there is internuclear ophthalmoplegia, where is the lesion?

A

Medial longitudinal fasciculus

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117
Q

If there is a conjugate lateral gaze disorder, where is the lesion?

A

CN 6

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118
Q

Examples of focal weakness in MS

A
  • Incontinence
  • Horner’s syndrome
  • Facial nerve palsy
  • Limb paralysis
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119
Q

Exames of focal sensory deficit in MS

A
  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia
  • Lhermitte’s sign (electric shock sensation down spine and into limbs when flexing neck)
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120
Q

What lesion causes Lhermitte’s sign?

A

Cervical spinal cord in dorsal column

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121
Q

Examples of symptoms of cerebellar lesions in MS

A
  • Sensory ataxia (positive Romberg’s test)
  • Dysarthria
  • Intention tremor
  • Nystagmus
  • Vertigo
  • Clumsiness
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122
Q

How is MS diagnosed?

A

McDonald criteria: 2 independent clinical attacks (time) and 2 separate lesions on MRI (space)

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123
Q

Investigations to support MS diagnosis

A
  • MRI of brain and spine (plaques)
  • Lumbar puncture for CSF (oligoclonal bands and increased IgG)
  • Evoked potentials: somatosensory, visual and motor (slow)
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124
Q

What is in the CSF of someone with MS?

A

Oligoclonal bands and increased IgG

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125
Q

Management of MS

A
  • MDT - neurologists, specialist nurses, PT/OT
  • Steroids: methylprednisolone + PPI gastroprotection
  • Disease-modifying drugs: interferon beta, monoclonal antibodies (alemtuzumab, natalizumab), latiramer acetate, fingolimod
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126
Q

Management of MS flare ups with optic neuritis

A

High-dose IV methylprednisolone

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127
Q

Managements to help with spasticity in MS

A
  • Stretching, PT, splinting
  • Baclofen
  • Gabapentin
  • Botox
  • Cannabis
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128
Q

Management of urinary symptoms in MS

A
  • Antimuscarinics - oxybutynin, solifenacin
  • Intermittent self-catheterisation or long-term catheters
  • Botox
  • Bladder training exercises
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129
Q

Management of pain in MS

A
  • Amitriptyline
  • Gabapentin
  • Pregabalin
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130
Q

Management of pain with trigeminal neuralgia or Lhermitte’s (MS)

A

Carbamazepine

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131
Q

Drug to improve walking speed in adults with MS

A

Fampridine

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132
Q

Which course of MS has the best and worst prognosis?

A

Best = relapse remitting MS
Worst = primary progressive MS

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133
Q

Difference beween a head injury and traumatic brain injury

A

Head injury is any trauma to the head
TBI needs evidence of damage to the brain as a result of trauma to the head, presenting as a reduced GCS or presence of focal neurological deficit
All TBIs are head injuries, but not all head injuries are TBIs

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134
Q

Mechanisms of traumatic brain injuries

A
  • Shearing and rotational stresses on decelerating brain
  • Direct trauma to neurones and axons
  • Brain oedema and raised intracranial pressure
  • Brain hypoxia
  • Brain ischaemia
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135
Q

Risk factors for TBI

A
  • Road traffic accidents
  • Excessive alcohol use
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136
Q

GCS for minimal, mild, moderate and severe head injury

A
  • Minimal = GCS 15 with no LOC
  • Mild = 13-15 with concussion
  • Moderate = 9-12
  • Severe = 3-8
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137
Q

Presentation of mild TBI

A
  • Stunned or dazed for seconds to minutes
  • Post-traumatic amnesia
  • Headache
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138
Q

Presentation of more serious TBIs

A
  • Unconscious (GCS <5 at 24 hours)
  • Post-traumatic amnesia lasting longer
  • Unable to lay down any continuous memory
  • Intermittent restlessness or lethargy during first few weeks
  • Focal deficits, e.g. hemiparesis or aphasia
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139
Q

What is Parkinson’s disease?

A

Neurodegenerative disorder characterised by loss of dopaminergic neurones (and so reduction of dopamine) within the substantia nigra pars compacta of the basal ganglia, leading to disorders of movement

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140
Q

Pathophysiology of Parkinson’s disease

A

Loss of dopaminergic neurones in the substantia nigra pars compacta leads to progressive reduction of dopamine in the basal ganglia
Lack of dopamine causes loss of communication between the basal ganglia, thalamus and motor cortex and impaired control of voluntary movement
Lewy bodies in dopaminergic neurones of SNPC

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141
Q

Risk factors for Parkinson’s disease

A
  • Increasing age
  • Male
  • Family history
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142
Q

Prodromal pre-motor symptoms of Parkinson’s disease

A
  • Anosmia
  • REM sleep behaviour disturbance
  • Insomnia
  • Daytime sleepiness
  • Depression and anxiety
  • Aches, pains and cramping
  • Autonomic: orthostatic hypotension, constipation, urinary frequency and incontinence, sweating, hypersalivation and drooling
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143
Q

4 core symptoms of Parkinsonism

A
  • Bradykinesia
  • Resting tremor
  • Rigidity
  • Postural instability
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144
Q

Examples of bradykinesia in Parkinson’s disease

A
  • Reduced dexterity - problems doing up buttons and typing
  • Festinant gait (shuffling, pitched forward), reduced arm swing, freezing at obstacles or doors
  • Micrographia
  • Hypomimia
  • Serpentine stare
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145
Q

What type of tremor is seen in Parkinson’s?

A

Resting tremor
Pill-rolling
Improves on voluntary movement

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146
Q

Types of rigidity in Parkinson’s

A
  • Cogwheel (resistance to passive movement)
  • Lead-pipe (stiffness through entire movement)
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147
Q

What is the progression of symptoms in Parkinson’s usually?

A
  • Prodromal pre-motor symptoms
  • Motor symptoms starting unilaterally and becoming bilateral
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148
Q

How is Parkinson’s disease diagnosed?

A

Clinical diagnois - UK PDS Brain Bank Criteria

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149
Q

What imaging can be useful in Parkinson’s?

A

Dopamine transporter (DAT) imaging using single-photon emission CT (SPECT) or PET scan

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150
Q

Differentials for Parkinson’s disease

A
  • Vascular Parkinsonism
  • Normal pressure hydrocephalus
  • Pressure on substantia nigra from tumour/bleed/abscess
  • Antipsychotics
  • Cerebellar ataxia
  • Wilson’s disease
  • Encephalitis and neurosyphilis
  • Parkinson’s plus
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151
Q

4 Parkinson’s plus diseases

A
  • Multiple system atrophy
  • Progressive supranuclear palsy
  • Lewy body dementia
  • Corticobasal degeneration
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152
Q

How is Parkinson’s tremor different from benign essential tremor?

A
  • Asymmetrical
  • Slower
  • Worse at rest
  • Improves with intentional movement
  • Other Parkinson’s features
  • No change with alcohol
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153
Q

Drugs for Parkinson’s disease

A
  • Synthetic dopamine
  • Dopamine agonist
  • Monoamine oxidase B (MAO-B) inhibitor
  • Catechol-O-methyltransferase (COMT) inhibitor
  • Amantadine
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154
Q

2 synthetic dopamines

A
  • Levodopa
  • Carbidopa
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155
Q

Ways of taking synthetic dopamine

A
  • Dispersible (rescue/morning)
  • Standard release (daytime)
  • Slow release (night)
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156
Q

What can be taken with levodopa to prevent breakdown before it reaches the brain?

A

Peripheral decarboxylase inhibitor: benserazide and carbidopa
(co-beneldopa and co-careldopa respectively)

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157
Q

What is Stalevo?

A
  • Levodopa (synthetic dopamine)
  • Carbidopa (symthetic dopamine and peripheral decarboxylase inhibitor)
  • Entacapone (catechol-O-methyltransferase inhibitor)
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158
Q

4 non-ergot derived dopamine agonists

A
  • Pramipexole
  • Ropinirole
  • Rotigotine
  • Apomorphine
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159
Q

Important side effect of dopamine agonists

A

Dopamine dysregulation syndrome - impulse control disorder and obsessions

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160
Q

How can apomorphine be taken?

A
  • Subcutaneous
  • Infusion
  • Rescue treatment (pen)
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161
Q

3 ergot-derived dopamine agonists

A
  • Bromocriptine
  • Pergolide
  • Cabergoline
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162
Q

2 monoamine oxidase B (MAO-B) inhibitors

A
  • Selegiline
  • Rasagiline
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163
Q

Dangers and contraindications with monoamine oxidase B (MAO-B) inhibitor

A
  • Serotonin syndrome with SSRI and tricyclics
  • Tramadol, pethidine and methadone contraindicated
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164
Q

2 catetchol-O-methyltransferase (COMT) inhibitors

A
  • Entacapone
  • Opicapone
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165
Q

Non-pharmacological management of Parkinson’s

A
  • MDT - PD nurse specialist, OT, PT, SALT and dietician
  • Palliative care and end of life planning
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166
Q

Treatment of REM sleep behavioural disorder in PD

A
  • Clonazepam
  • Melatonin
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167
Q

Treatment of daytime sleepiness in PD

A
  • Medication review
  • Modafinil
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168
Q

Treatment of nighttime akinesia in PD

A
  • Medication review
  • Levodopa
  • Rotigotine patch (dopamine agonist)
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169
Q

Treatment of postural hypotension in PD

A
  • Medication review and stop antihypertensives
  • Midodrine
  • Fludrocortisone
  • Ephedrine
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170
Q

Treatment of urinary frequency in PD

A

Anticholinergics

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171
Q

Treatment of constipation in PD

A

Trospium

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172
Q

Treatment of hypersalivation in PD

A
  • Hyoscine
  • Glycopyrrolate
  • Botox
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173
Q

Treatment of dementia in PD

A
  • Acetylcholinesterase inhibitor
  • Memantine
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174
Q

Treatment of psychosis in PD

A
  • Assess for provoking factors (medical illness, infection, metabolic disturbance)
  • Refer to neurology
  • Discontinue drugs (anticholinergics, amantadine, MOA inhibitors, dopamine agonist, levodopa)
  • Quetiapine
  • Clozapine
  • Acetycholinesterase inhibitors
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175
Q

Complications of PD

A
  • Freezing (sudden stoppage of movement)
  • Dyskinesia (levodopa) - dystonia, chorea and athetosis
  • Impulse control disorders (dopamine agonist)
  • Depression and anxiety
  • Depression
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176
Q

Complications of head injury

A
  • Death
  • Cognitive impairment
  • Hemipareis
  • Epilepsy (depressed skull fracture)
  • Post-traumatic syndrome: headache, dizziness and malaise
  • Benign paroxysmal positional vertigo
  • Chronic subdural haematoma
  • Hydrocephalus
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177
Q

Immediate management of head injury

A
  • Airway
  • If coma, depressed fracture or suspicion of intracranial haematoma: CT imaging and discussion with neurosurgical unit
  • Assisted ventilation in severe TBI
  • Intracranial pressure monitoring
  • Consider referral to neurosurgery
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178
Q

When should you refer a head injury to neurosurgery?

A
  • Significant abnormality on imaging
  • GCS 8 or less after resuscitation or drop in GCS after admission
  • Unexplained confusion for over 4 hours
  • Focal neurological signs or seizures without full recovery
  • Suspected penetrating injury or evidence of CSF leak
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179
Q

Management of depressed skull fracture

A

Surgical elevation and debridement

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180
Q

Management of linear fractures of vault or base

A

Heal spontaneously

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181
Q

Investigation for head injury

A

CT head +/- cervical spine

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182
Q

Indications for a CT head within an hour following head injury

A
  • GCS < 13 on first assessment or < 15 at 2 hours after injury
  • Signs of basal skull fracture or open or depressed skull fracture
  • Seizure or > 1 episode of vomiting
  • Focal neurological deficit
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183
Q

Indications for a CT head within 8 hours following head injury

A

On anti-coagulant or suffered loss of conscioussness/memory loss AND:
* Aged over 65
* Previous bleeding disorder
* Dangerous mechanism of injury, e.g. cyclist v vehicle or fall from height > 1m
* More than 30 minutes of retrograde amnesia of events before the head injury

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184
Q

Red flags of head injury

A
  • Impaired consciousness level
  • Dilated pupils which do not respond to light
  • Signs of basal skull fracture
  • Focal neurological deficit or visual disturbances
  • Seizures or amnesia
  • Significant headache or N+V
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185
Q

How soon upon arrival should a person with head injury be examined? Why?

A

15 minutes
Determine if they have serious brain or spinal injury

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186
Q

What should you do if someone is suspected to have a cervical spine injury?

A

Immobilisation of cerbical spine via semi-rigid collar, blocks and tape

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187
Q

Signs of basal skull fracture

A
  • Racoon eyes (bruising around eyes)
  • Battle’s sign (bruising behind ears)
  • CSF rhinorrhoa or otorrhoea (clear discharge from nose or ear)
  • Blood bulging from middle (haemotympanum)
  • Obvious penetrating injury
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188
Q

What is a brain abscess?

A

Focal bacterial infection

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189
Q

How common is a brain abscess?

A

10x rarer than a brain tumour in the UK

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190
Q

Causes of brain abscess

A
  • Bacteria: streptococcus anginosus, bacteroides species and staphylococci
  • HIV
  • Fungi
  • Parameningeal infective focus or distant source (lung, heart, abdo)
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191
Q

Presentation of brain abscess

A
  • Headache
  • Focal signs: hemiparesis, aphasia, hemianopia
  • Epilepsy
  • Fever
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192
Q

Management of brain abscess

A
  • High-dose antibiotics
  • Surgical resection or decompression
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193
Q

Investigations for brain abscess

A
  • Urgent MRI
  • Neurosurgical aspiration with stereotactic guidance
  • Bloods (raised ESR, leucocytosis)
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194
Q

What would a brain abscess look like on MRI?

A

Ring-enhancing mass, with considerable surrounding oedema

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195
Q

What is shingles caused by?

A

Viral infection caused by reactivation of varicella zoster virus (herpes zoster)
VZV lays dormant in dorsal root ganglia following resolution of chickenpox and if immunosuppressed the virus may reactivate

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196
Q

Risk factors for shingles

A
  • Increasing age
  • Immunosuppressed: systemic disease, cancer, post-transplantation, chemotherapy, high-dose steroids
  • Transplant recipients
  • Autoimmune disease
  • HIV infection
  • Co-morbid conditions: CKD, COPD, DM
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197
Q

Presentation of shingles

A
  • Prodromal paraesthesia and pain (throbbing, burning, stabbing) in affected dermatome
  • Unilateral erythematous maculopapular rash which doesn’t cross the midline
  • Clusters of vesicles
  • Pustules, which burst and crust over
  • Systemic features: headache, fever, malaise, fatigue
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198
Q

How is shingles diagnosed?

A

Clinical diagnosis based on appearance of rash

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199
Q

How is shingles with an atypical presentation diagnosed?

A

Swab from suspected lesion for PCR testing

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200
Q

What investigations may you do for someone with shingles?

A

Immunosuppression testing:
* HIV testing
* Immunoglobulins
* Cancer assessment

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201
Q

Management of shingles

A
  • Oral anti-viral therapy (aciclovir) within 72 hours of rash onset
  • Simple analgesia (paracetamol, NSAIDs) or neuropathic agents (amitriptyline, gabapentin)
  • Severe shingles, complications (meningitis/encephalitis) or significant immunosuppression: admission for IV antiviral therapy and monitoring
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202
Q

How long do people with shingles remain infectious?

A

Until all lesions have crusted over (5-7 days)

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203
Q

Prevention of shingles

A
  • Varicella zoster immunoglobulin for pregnant women (< 20 weeks) who have had significant exposure to chickenpox or shingles, or for severe neonatal infections
  • Shingles vaccination for those over 70
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204
Q

Complications of shingles

A
  • Scarring
  • Post-herpetic neuralgia
  • Secondary bacterial infection
  • Ramsay Hunt syndrome
  • Herpes zoster ophthalmicus
  • Motor neuropathy
  • CNS involvement: encephalitis, meningitis, myelitis
  • Disseminated infection
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205
Q

Findings on an MRI of brain and spine of someone with MS

A
  • Periventricular lesions
  • Callosal lesions
  • Juxtacortical lesions
  • Dawson’s fingers
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206
Q

How do steroids and disease-modifying drugs help with MS?

A

Steroids: reduce length of time of relapse
DMD: reduce number of relapses

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207
Q

What is muscular dystrophy?

A

Progressive degeneration of skeletal (and sometimes cardiac) muscle

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208
Q

What are the 1st and 2nd most common muscular dystrophies?

A
  1. Duchenne’s muscular dystrophy (DMD)
  2. Becker’s muscular dystrophy
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209
Q

Name types of muscular dystrophies

A
  • Duchenne’s muscular dystrophy
  • Becker’s muscular dystrophy
  • Myotonic dystrophy
  • Facioscapulohumeral muscular dystrophy
  • Oculopharyngeal muscular dystrophy
  • Limb-girdle muscular dystrophy
  • Emery-Dreifuss muscular dystrophy
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210
Q

What is the pathophysiology of muscular dystrophy?

A

X-linked recessive
Mutation in dystrophin gene
Deficiency of dystrophy causes sarcolemma (cell membrane) to wilt and become unstable
CK escapes and calcium enters, leading to cell death

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211
Q

Why is Duchenne’s muscular dystrophy worse than Becker’s muscular dystrophy?

A

In DMD there is an absence of dystrophin, whereas in Becker’s there are low levels of dystrophin

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212
Q

In muscular dystrophy, what happens to the muscle short-term vs long-term?

A

Short-term: muscle generation resulting in muscle fibres of different sizes
Long-term: muscle atrophy and infiltration by fat and fibrotic tissue

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213
Q

Risk factors for muscular dystrophy

A
  • Designated male at birth
  • Family history
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214
Q

How does the age of presentation vary for Duchenne’s and Becker’s muscular dystrophy?

A

DMD: 3-5
Becker’s: 8-12

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215
Q

Clinical manifestations of muscular dystrophy

A
  • Start walking later
  • Waddling gait
  • Difficulty running
  • Difficulty rising to their feet
  • Pelvic muscle weakness
  • Gower’s sign (downward dog, hands climb up their legs to stand)
  • Calf pseudohypertrophy (fat and fibrotic tissue)
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216
Q

When would you expect someone with muscular dystrophy to require a wheelchair?

A

DMD: wheelchair bound in teenage years
Becker’s: some require wheelchairs in late 20s-30s, others able to walk without assistance into late adulthood

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217
Q

How is muscular dystrophy diagnosed?

A
  • Creatinine kinase grossly elevated
  • Muscle biopsy shows variation in muscle fibre size, necrosis, regeneration and replacement by fat; absence of dystrophin on immunochemical staining
218
Q

Management of muscular dystrophy

A
  • Medications: oral corticosteroids, creatine supplementation
  • Physical: wheelchair, brace, respiratory support, surgery for contractures/scoliosis
  • MDT: PT, OT
219
Q

How to prevent muscular dystrophy

A

Genetic counselling
* Prenatal diagnosis
* Carrier detection (females with affected brother have 50% chance of carrying DMD gene)

220
Q

Complications of muscular dystrophy

A
  • Respiratory failure
  • MSK problems: joint contractures, chest deformities, spinal deformities (scoliosis)
  • Dilated cardiomyopathy and arrhythmias
221
Q

Life expectancy of someone with muscular dystrophy

A

DMD: 25-35
Becker’s: better

222
Q

Causes of proximal myopathy

A
  • Infection: HIV, EBV, hepatitis, bacterial pyomyositis, Lyme disease, toxoplasmosis, candida
  • Autoimmune: SLE, vasculitis, rheumatoid arthritis, systemic sclerosis, polymyositis/dermatomyositis
  • Metabolic: hypo/hyperkalaemia, hypermagnesemia
  • Iatrogenic: statins, corticosteroids, amiodarone, colchicine
  • Neoplastc: carcinomatous neuromyopathy
  • Congenital myopathies
  • Degenerative: muscular dystrophies
  • Endocrine: hypo/hyperthyroidism, hyperparathyroidism, Addison’s disease, Cushing’s syndrome
  • Other: alcohol, rhabdomyolysis, sarcoidosis, mitochondrial myopathy
223
Q

Clues that proximal myopathy has a metabolic cause

A
  • Difficulties with exercise
  • Cramps and myalgia
  • Episodes of weakness come and go
224
Q

Clues that proximal myopathy is caused by mitochondrial myopathy

A

Other symptoms with heart, brain, GI tract, etc.

225
Q

Risk factors for proximal myopathy

A
  • Family history of myopathy
  • Designated male at birth (X-linked)
  • Autoimmune, metabolic or endocrine disorder
  • Exposure to certain medications or toxins
226
Q

Hair, chair and stairs

Symptoms of proximal myopathy

A
  • Difficulty performing ADLs (bathing, dressing, combing hair)
  • Trouble getting out of chair, climbing stairs or performing tasks that require reaching over your head
  • Falls
  • Muscle cramps or spasms
  • Muscle fatigue with activity
  • Shortness of breath with exertion
227
Q

Signs of proximal myopathy

A
  • Muscle wasting
  • Reduced power
  • Trouble standing from sitting and raising arms above head
  • In fetus: decreased movements
  • In neonates: floppy
  • In toddlers: motor delays (walking, hopping, running, climbing stairs, grasping a spoon/pencil)
228
Q

Causes of proximal muscle weakness that isn’t proximal myopathy

A
  • Neurological: MND, GBS, myasthenia gravis, cerebral palsy, spinal muscular atrophy
  • Not true weakness: polymyalgia rheumatica, fibromyalgia, osteoarthritis, rotator cuff problems, fatigue/malaise/depression
229
Q

Investigations for proximal myopathy

A
  • Bloods: U&E, Ca, P, Mg; CK; TFT; rheumatological screen (ESR, ANA, RF)
  • Nerve conduction studies and EMG
  • MRI muscle
  • Muscle biopsy
230
Q

What is myasthenia gravis?

A

Autoimmune disorder against acetylcholine receptors of the postsynaptic membrane at the neuromuscular junction

231
Q

What ages most commonly get myasthenia gravis?

A

Women during 20s-30s
Men during 50s-60s

232
Q

What causes myasthenia gravis?

A

Autoimmune disease
Caused most commonly by acetylcholine receptor antibodies, which block the AChR and prevent stimulation by ACh, and activate the complement system leading to cell damage
Other antibodies (MuSK and LRP4 antibodies) destroy proteins involved in creation and organisation of AChR

233
Q

Why do symptoms depend on muscle activity in myasthenia gravis?

A

With increased muscle activity, more receptors are used and become blocker, so there is less effective stimulation of muscle
With rest, receptors are cleared and symptoms improve

234
Q

Risk factors for myasthenia gravis

A
  • Female
  • Family history
  • Other autoimmune diseases
  • Thymoma
235
Q

Clinical manifestations of myasthenia gravis

A

Weakness that worsens with activity and improves with rest
* Proximal muscles: difficulty climbing stairs, standing from sitting and raising hands above head
* Ocular muscles: diplopia and ptosis
* Neck and facial muscles: myasthenia snarl, fatigue in jaw when chewing, head drop, dysarthria and dysphagia
* Respiratory: shortness of breath

236
Q

How can you exacerbate signs in myasthenia gravis?

A
  • Prolonged blinking - ptosis
  • Prolonged upward gazing - diplopia
  • Repeated abduction of one arm 20 times - unilateral weakness when comparing both sides
237
Q

What scar should you check for in someone with suspected myasthenia gravis?

A

Thymectomy scar

238
Q

What are the investigations for myasthenia gravis?

A
  • Antibodies: AChR, MuSK and LPR4 antibodies
  • CT chest (thymoma)
  • Electromyography with repetitive nerve stimulation
  • Tensilon test (edrophonium improves muscle weakness)
  • Ice pack test (onto closed eyelid for minute improves symptoms)
239
Q

Management of myasthenia gravis

A
  • Acetylcholinesterase inhibitors: pyridostigmine and neostigmine
  • Immunosuppressants: prednisolone, azathioprine and methotrexate
  • Rituximab (monoclonal antibody)
  • Thymectomy
240
Q

Management of myasthenic crisis

A
  • Non-invasive ventilation
  • IV immunoglobulins or plasmapheresis
241
Q

What should be monitored in someone with myasthenia gravis?

A
  • Forced vital capacity
  • Bulbar function
242
Q

Complications of myasthenia gravis

A
  • Myasthenic crisis
  • Respiratory failure
  • Aspiration pneumonia
  • Thymus dysfunction
243
Q

What is myasthenic syndrome?

A

Disorder of the neuromuscular junction

244
Q

Causes of myasthenic syndrome

A
  • Myasthenia gravis
  • Lambert-Eaton myasthenic syndrome
  • Congenital myasthenia
245
Q

Risk factors for myasthenic syndrome

A
  • Family history
  • Other autoimmune diseases
  • Thymoma (myasthenia gravis)
  • Cancer, particularly small cell lung cancer (Lambert-Eaton)
246
Q

Symptoms of myasthenic syndrome

A

Weakness
* Proximal musce weakness: ‘hair, chair and stairs’
* Ocular muscle weakness: diplopia and ptosis
* Facial muscle weakness: dysarthria and dysphagia

247
Q

Signs of Lambert-Eaton syndrome

A
  • Reduced power
  • Reduced tendon reflexes (cardinal sign), with improvement following a period of strong muscle contraction
248
Q

Differential diagnoses of myasthenic syndrome

A
  • Botulism
  • Myopathy
  • Chronic inflammatory demyelinating neuropathy
  • GBS
249
Q

Investigations for myasthenic syndrome

A
  • Antibodies: AChR, MuSK, LRP4 antibodies (myasthenia gravis) and voltage-gated Ca channel antibodies (Lambert-Eaton)
  • Nerve conduction studies and electromyography with repetitive nerve stimulation
  • CXR (small cell lung cancer in Lambert-Eaton) and CT chest (thymoma in myasthenia gravis)
250
Q

Management of myasthenic syndrome

A
  • Pyridostigmine
  • Immunosuppressants: prednisolone and azathioprine
  • Ventilation and IV immunoglobulins/plasmapheresis
251
Q

Complications of myasthenic syndrome

A
  • Respiratory failure
  • Aspiration pneumonia
252
Q

What is radiculopathy?

A

Injury or damage to the spinal nerve or its root where it leaves the spine

253
Q

Causes of radiculopathy

A

V - vasculitis
I - epidural abscess, osteomyelitis (TB > Pott’s disease)
T - injury, compression fractures
A - acute/chronic inflammatory demyelinating polyradiculopathy
N - intradural tumour, metastasis, myeloma, lymphoma
D - spinal canal stenosis, spondylosis, osteoarthritis (osteophytes)
E - DM
O - slipped disc, spondylolisthesis, scoliosis

254
Q

Risk factors for radiculopathy

A
  • Inactive
  • Overweight
  • Poor posture
  • Lifting heavy objects
  • Operating vibrating equipment
  • Trauma
255
Q

Clinical manifestations of radiculopathy

A
  • Sharp, shooting, radiating pain
  • Numbness or tingling
  • Weakness
  • Reduced reflexes
256
Q

L1 radiculopathy

A

S - inguinal region
P - hip flexion (uncommon)

257
Q

L2-4

A

P - back into anterior thigh
S - anterior thigh and medial lower leg (patella)
P - hip flexion and adduction, knee extension and ankle dorsiflexion
R - knee

258
Q

L5

A

P - back into lateral aspect of leg to foot (big toe)
S - lateral aspect of lower leg and dorsum of foot
P - ankle dorsiflexion, big toe extension and ankle inversion/eversion

259
Q

S1

A

P - back into posterior aspect of leg into foot
S - posterior leg and lateral foot (5th toe)
P - ankle plantarflexion, hip extension and knee flexion
R - ankle

260
Q

S2

A

P - ankle plantarflexion, pelvic floor

261
Q

S5

A

S - perianal region

262
Q

C5

A

P - neck, shoulder and scapula
S - lateral aspect of upper arm
P - shoulder abduction and elbow flexion
R - biceps and brachioradialis

263
Q

C4

A

S - clavicle
P - shoulder elevation

264
Q

C6

A

P - neck, shoulder, scapula, lateral arm, forearm and hand
S - lateral forearm, thumb and finger (thumb)
P - elbow flexion and supination/pronation
R - biceps and brachioradialis

265
Q

C7

A

P - neck, shoulder, hand and middle finger
S - palm, middle and index fingers (middle finger)
P - elbow, finger and wrist extension
R - triceps

266
Q

C8

A

P - neck, shoulder, medial forearm, hand and 4th/5th fingers
S - medial forearm, hand and 4th/5th ginger
P - elbow extension and finger flexion

267
Q

T1

A

P - finger adduction

268
Q

Thoracic

A

P - to chest and abdomen

269
Q

T4

A

S - nipple

270
Q

T10

A

S - umbilicus

271
Q

T12

A

Inguinal region

272
Q

Special test for L2-4 radiculopathy

A

Reverse straight leg raise (extend hip while in prone)

273
Q

Special test for L5/S1 radiculopathy

A

Straight leg raise (raise leg with knee extended)

274
Q

Special tests for cervical radiculopathy

A
  • Lhermitte phenomenon (neck flexion = shock-like paraesthesia down spine)
  • Shoulder abduction relief test (arm of affected side raised and hand placed on head = relief)
  • Spurling manoeuvre (downward pressure on head when extended and rotated to affected side = worse)
275
Q

Investigations for radiculopathy

A
  • MRI/CT
  • X-ray
  • EMG and NCS
  • Myelography
  • Blood tests: ESR/CRP, FBC, glucose, vitamins
276
Q

Conservative management of radiculopathy

A
  • Rest
  • Activity modification
  • Physio
  • Weight loss
277
Q

Medical management of radiculopathy

A
  • NSAIDs (ibuprofen, aspirin, naproxen)
  • Opioids
  • Amitriptyline, pregabalin, gabapentin
  • Muscle relaxants: benzodiazepine (diazepam), baclofen
  • Corticosteroids PO or injections into spine
278
Q

Surgeries for radiculopathy

A
  • Spinal decompression surgery: discectomy, laminectomy
  • Spinal fusion
  • Foraminotomy
  • Disc replacement surgery
279
Q

What is chorea?

A

Involuntary, irregular or unpredictable muscle movements, affecting the arms, legs and facial muscles

280
Q

Causes of chorea

A

V - stroke
I - rheumatic fever/post-strep infection, AIDS
A - SLE, MS, antiphospholipid syndrome
M - hypoglycaemia, kernicterus (bilirubin)
I - levodopa, antipsychotics
N - brain tumour near basal ganglia
C - benign hereditary chorea
D - Huntington’s, Parkinson’s, Wilson’s
E - thyrotoxicosis
O - cocaine, amphetamines, carbon monoxide, pregnancy

281
Q

What is Sydenham chorea?

A

Chorea caused by rheumatic fever or post-streptococcal infection

282
Q

What is tardive dyskinesia?

A

Chorea caused by antipsychotics

283
Q

What is chorea gravidarum?

A

Chorea caused by pregnancy

284
Q

Risk factors for chorea

A
  • Family history of Huntington’s
  • Rheumatic fever, infection or head injury in childhood
  • Autoimmune condition
  • Over 40
285
Q

Symptoms of chorea

A
  • Involuntary arm/leg/face movements (fidget, twist, jerk)
  • Milkmaid’s grip
  • Move tonue in and out of mouth
  • Abnormal gait
286
Q

Medication for tardive dyskinesia

A

Tetrabenazine

287
Q

Treatment for chorea caused by levodopa

A

Change to amantadine

288
Q

Treatment of rheumatic fever

A

Corticosteroids and antibiotics

289
Q

Management of chorea caused by dopamine

A
  • Adjust or reduce dose
  • Spread dose out
  • Use extended-release formulations
290
Q

Management of brain tumour

A

Surgery to remove tumour

291
Q

Complications of chorea

A
  • Difficulty swallowing foods and drinks
  • Behavioural or emotional challenges
  • Physical injury
  • Social stigmatisation
292
Q

Risk factors for Huntington’s

A
  • Family history
  • Middle age
293
Q

Cause of Huntington’s

A

Autosomal dominant trinucleotide (CAG > glutamine) repeats over 35 times, resulting in mutation in huntingtin (HTT) gene on chromosome 4
Mutated protein aggregates in putamen and caudate of basal ganglia causing neuronal cell death and loss of brain tissue, which results in decreased GABA and ACh, and increased dopamine

294
Q

What is the penetrance of Huntington’s?

A

Reduced penetrance with 36-39 repeats
100% penetrance with over 40 repeats

295
Q

Why do successive generations affected by Huntington’s have earlier onset and worse disease?

A

Anticipation: expansion of trinucleotide repeat during meiosis

296
Q

Why is anticipation of Huntington’s disease worse when inherited from father?

A

Expansion of trinucleotide repeat during meiosis worse in spermatogenesis

297
Q

Clinical manifestations of Huntington’s

A

Insidious, progressive worsening of symptoms from around 40
* Psychiatric - dementia, depression, personality changes
* Movement - chorea, athetosis, abnormal eye movements, dysarthria, dysphagia

298
Q

Investigations for Huntington’s

A
  • Genetic test
  • CT/MRI brain
299
Q

Medications for Huntington’s

A
  • Antipsychotics: risperidone, sulpiride, olanzapine
  • Tetrabenazine
  • Amantadine
  • Benzodiazepine (aggression)
  • Sertraline (depression)
300
Q

MDT approach to Huntington’s

A
  • OT
  • PT
  • Psychologist
  • SALT
301
Q

Counselling for those with Huntington’s

A
  • Genetic counselling regarding relatives, pregnancy and children
  • Advanced directives to document their wishes as the disease progresses
  • End of life care planning
302
Q

Prognosis of Huntington’s

A

Life expectancy 10-20 years after symptom onset
Death usually from aspiration pneumonia or suicide

303
Q

When someone presents with radiculopathy, what should you think about red flags for?

A
  • Cauda equina syndrome
  • Infection
  • Fracture
  • Malignancy
  • Metastatic disease
304
Q

With someone presenting with radiculopathy, what are red flags for cauda equina syndrome?

A
  • Faecal incontinence
  • Urinary retention (painless, with secondary overflow incontinece)
  • Saddle anaesthesia
305
Q

With someone presenting with radiculopathy, what are red flags for infection?

A
  • Immunosuppression
  • IV drug abuse
  • Unexplained fever
  • Chronic steroid use
306
Q

With someone presenting with radiculopathy, what are red flags for fracture?

A
  • Chronic steroid use
  • Significant trauma
  • Osteoporosis
  • Metabolic bone disease
307
Q

Symptoms of spinal claudication

A

Bilateral radiating leg pain or paraesthesia that comes on with walking and is such that they have to stop and rest for a number of minutes before walking again, symptoms relieved by leaning forward

308
Q

What is myelopathy?

A

Spinal cord compression causing nerves not to work properly

309
Q

Causes of myelopathy

A

V - haematoma
I - epidural abscess, osteomyelitis, discitis
T - spinal injury
A - rheumatoid arthritis
M - B12 deficiency
I - radiation
N - primary bone tumours, metastases, structural weakness secondary to cancer
C - congenital stenosis
D - spondylosis > osteophytes, spinal stenosis, Parkinson’s, amyotrophic lateral sclerosis
O - prolapsed disc, spinal cyst

310
Q

What is subacute combined degeneration of the spinal cord?

A

Demyelination of lateral and posterior columns of the spinal cord, commonly due to vitamin B12 deficiency

311
Q

Most common cancers to metastasise to the spine

A
  • Kidney
  • Prostate
  • Breast
  • Lung
  • Thyroid
  • Multiple myeloma
312
Q

Risk factors for myelopathy

A
  • Cancer
  • Heavy lifting
  • Overweight
  • Smoking
  • Inactive
  • Scoliosis
313
Q

Symptoms of myelopathy

A
  • Neck, arm, leg or back pain
  • Tingling, numbness or weakness
  • Loss of fine finger movements
  • Difficulty walking
  • Loss of urinary or bowel control
  • Issues with balance and coordination
314
Q

Investigations for myelopathy

A
  • X-ray
  • MRI
  • Myelogram
  • Electromyogram or evoked potentials
  • Blood tests: FBC, ESR, B12, U&E, syphilis, LFT, PSA
  • CXR (lung cancer)
315
Q

Signs of myelopathy

A

UMN signs
* Spastic gait
* Hypertonia
* Hyperreflexia
* Babinski sign
* Clonus
* Cross-adductors
* Hoffman’s sign
* Deltopectoral reflex
* Sensory loss

316
Q

Management of myelopathy

A

Spinal decompression surgery (discectomy, laminectomy, laminoplasty, decompression and spinal fusion)

317
Q

Conservative management of myelopathy

A
  • NSAIDs
  • Corticosteroids PO or injection
  • Brace
  • Physical therapy
  • Hot and cold treatments
  • Acupuncture and chiropractic care
318
Q

Treatment of spinal malignancy causing cord compression

A

IV dexamethasone and radiotherapy

319
Q

Treatment of epidural abscess causing cord compression

A

Antibiotics

320
Q

Complications of myelopathy

A

Paralysis

321
Q

What causes spinal muscular atrophy?

A

Mutation in SMA1 gene

322
Q

Clinical manifestation of spinal muscular atrophy

A

Proximal, symmetrical muscle weakness
Legs more than arms
Can affect bulbar function and breathing

323
Q

Presentation of type 1 spinal muscular atrophy

A

First 6 months
* Weak and floppy arms and legs
* Problems moving, eating, breathing and swallowing
* Unable to raise head

324
Q

Presentation of type 2 spinal muscular atrophy

A

7-18 months
* Can sit, can’t stand
* Weak arms or legs
* Shaking in fingers and hands
* Joint problems (scoliosis)
* Weak breathing muscles and trouble coughing

325
Q

Presentation of type 3 spinal muscular atrophy

A

After 18 months
* Able to stand and walk, but may find walking and getting up from sitting difficult and may lose ability to walk
* Balance problems
* Difficulty running or climbing steps
* Shaking in their fingers

326
Q

Presentation of type 4 spinal muscular atrophy

A

Early adulthood
* Weakness in hands and feet
* Difficulty walking
* Shaking and twitching muscles

327
Q

What is somatic symptom disorder?

A

Symptoms suggestive of a physical disorder, but in the absence of physiological illness, e.g. pins and needles, headaches, visual disturbances

328
Q

Clues that it might be a somatic symptom disorder

A
  • Prolonged history of multiple physical symptoms, often occurring in different systems, that cannot be explained by any detectable physical disorder
  • Belief that they have a serious illness
  • Repeated medical consultations and requesting investigations
  • Do not accept reassurnace from doctors
329
Q

Causes of cranial neuropathy

A

V - aneurysm, ischaemia, stroke, vasculitis
I - Lyme disease, neurosyphilis, HIV
T
A - GBS, SLE, MS
M - Wernicke’s encephalopathy
I - surgery
N - brain tumour
E - DM

330
Q

Clinical manifestation of CN 1 neuropathy

A

Reduced smell and taste

331
Q

Where would the cancer and trauma be to cause CN 1 neuropathy?

A

Tumour: frontal lobe, ethmoid, meningioma of olfactory groove
Trauma: basal skull fracture, frontal fracture

332
Q

Causes of monocular sight impairment

A
  • MS
  • Giant cell arteritis
333
Q

Causes of bilateral hemianopia

A
  • Internal carotid artery aneurysm
  • Pituitary adenoma
  • Craniopharyngioma
334
Q

Causes of homonymous hemianopia

A
  • Stroke
  • Brain abscess
  • Brain tumour
335
Q

Causes of optic neuritis

A
  • Demyelination
  • Sinusitis
  • Syphilis
  • Collagen vascular disorders
336
Q

Clinical manifestation of CN 2 neuropathy

A
  • Visual field defects
  • Pupillary abnormalities
  • Pain on eye movement
337
Q

Causes of third nerve palsy

A

V - posterior communicating/carotid artery aneurysm, cavernous sinus thrombosis
I - syphilis, orbital cellulitis, invasive fungal sinusitis, meningitis
A - giant cell arteritis
N - meningeal carcinomatosis

338
Q

Clinical manifestation of third nerve palsy

A
  • Fixed dilated pupil, which doesn’t accommodate
  • ‘Down and out’ eye appearance
  • Diplopia
  • Ptosis
  • Internuclear ophthalmoplegia
  • Trouble moving eye
  • Pain
  • Loss of eye reflex
339
Q

How to prevent diplopia with third nerve palsy

A

Short-term: eye patch
Long-term: prisms and strabismus surgery

340
Q

Clinical manifestation of fourth nerve palsy

A
  • Diplopia
  • Eye(s) turn abnormally
  • Tilt head away from affected side
341
Q

Causes of fifth nerve palsy

A
  • Herpes zoster virus
  • Nasophrayngeal carcinoma
  • Acoustic neuroma
342
Q

Clinical manifestations

A
  • Numbness or dysaesthesia
  • Weakness of jaw clenching and side-to-side movement
  • Fasciculations of temporalis and masseter muscles
343
Q

Causes of sixth nerve palsy

A
  • Pontine cerebrovascular accident
  • Meningitis
  • Cavernous sinus thrombosis
  • Pituitary adenoma
344
Q

Clinical manifestation of sixth nerve palsy

A
  • Diplopia, worse on horizontal gaze in direction of lesion
  • Failed eye abduction, eye deviates medially
  • Strabismus
  • Blurred vision
  • Dizziness
  • Eye pain
345
Q

Causes of eighth nerve palsy

A
  • Loud noise
  • Paget’s disease of bone
  • Meniere’s disease
  • Herpes zoster virus
  • Neurofibroma, acoustic neuroma
  • Aminoglycosides, furosemide, aspirin
  • Lead
346
Q

Clinical manifestation of eighth nerve palsy

A
  • Unilateral sensorineural deafness
  • Tinnitus
  • Nystagmus
347
Q

Clinical manifestation of ninth nerve palsy

A
  • Hoarseness
  • Nasal speech
348
Q

Clinical manifestation of tenth nerve palsy

A
  • Hoarseness
  • Nasal speech
  • Quiet
  • Bovine cough
  • Palate moves asymmetrically when they say ‘ahhh’
349
Q

Clinical manifestation of eleventh nerve palsy

A

Weakness and wasting of sternocleidomastoid and trapezius muscles

350
Q

Clinical manifestation of twelfth nerve palsy

A

Ipsilateral
* Wasting of tongue
* Fasciculation of tongue
* Deviation on protrusion of tongue

351
Q

Investigations for cranial neuropathy

A
  • Bloods: FBC, CRP, glucose
  • EMG and NCS
  • CT/MRI brain
  • Biopses of skin and nerves
  • LP
  • Angiography
352
Q

Management of cranial neuropathy

A
  • Treat underlying cause (abx, surgery, anti-HTN, anti-DM)
  • Eat nutritious food
  • Don’t smoke and limit alcohol
353
Q

What is Bell’s palsy?

A

Unilateral facial nerve palsy

354
Q

Causes of Bell’s palsy

A
  • Infection: Lyme disease, polio, otitis media, herpes zoster virus, HIV
  • Skull fracture
  • Cerebellopontine angle or parotid tumour
355
Q

Clinical manifestation of Bell’s palsy

A
  • Unilateral facial weakness: loss of nasolabial fold, drooping eyebrow/corner of mouth, asymmetrical smile, speech/chewing difficulty
  • Ear pain
  • Incomplete eye closure
  • Drooling
  • Tingling in cheek and mouth
  • Hyperacusis
356
Q

Difference between stroke and Bell’s palsy

A

Bell’s palsy (LMN) has paralysis of forehead, stroke (UMN) does not

357
Q

What grades facial weakness?

A

House-Brackmann system

358
Q

How is Bell’s palsy diagnosed?

A

Clinically, based on unilateral facial weakness of rapid onset without forehead sparing

359
Q

Features that point to a different diagnosis than Bell’s palsy

A
  • Slow onset and progressive
  • Overt pain
  • Systemic illness
  • Vestibular abnormalities
  • Other hearing abnormalities
  • Forehead sparing (stroke)
  • Mass
  • Recurrent palsy
  • Bilateral involvement (sarcoidosis, GBS, Lyme disease, HIV)
360
Q

Management of Bell’s palsy

A
  • Prednisolone 50mg for 10 days, within 72 hours of onset
  • Straw for liquids, soft diet
  • Eye care: eye drops, tape eye when sleeping, sunglasses outdoors
361
Q

Prognosis of Bell’s palsy

A

Good, although may take several months to recover

362
Q

What is bulbar palsy?

A

Neuropathy of cranial nerves 9, 10 and 12

363
Q

Causes of bulbar palsy

A

Brainstem: infarction, syringobulbia, MND, tumour, central pontine myelinolysis
Skull base: nasopharyngeal carcinoma, neurofibroma, jugular venous thrombosis, trauma
Neck and nasopharynx: nasopharyngeal carcinoma, carotid artery dissection, trauma, lymph node biopsy in posterior triangle

364
Q

Clinical manifestation of bulbar palsy

A
  • Hoarse, nasal, quiet speech
  • Bovine cough
  • Palate moves asymmetrically when they say ‘ahhh’
  • Ipsilateral wasting of tongues, with fasciculations and deviation on protrusion of tongue
365
Q

What is cerebellar syndrome?

A

Cerebellar disease affecting co-ordination, balance and speech

366
Q

Causes of cerebellar syndrome

A

V - stroke, AV malformation
I - brain abscess, HIV, creutzfeldt-jakob disease
T
A - gluten ataxia, MS
M - chronic alcohol use, Wernicke’s encephalopathy, vitamin deficiencies (B12, E, folate)
I - antiepileptics, antipsychotics
N - medulloblastoma, paraneoplastic cerebellar degeneration
C - chiari malformation, cerebral palsy, spinocerebellar ataxias, Friedreich’s ataxia, ataxia telangiectasia
D - multiple system atrophy, superficial siderosis
E - hypothyroidism
O - lead/carbon monoxide poisoning

367
Q

Symptoms of cerebellar syndrome

A
  • Feels drunk
  • Difficulty walking
  • Dizzy
  • Clumsy
  • Diplopia
  • Dysphagia
  • Problems with dexterity
  • Vomiting
368
Q

DANISH

Signs of cerebellar syndrome

A
  • Dysdiadochokinesia or dysmetria
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Speech (slurred or scanning)
  • Hypotonia
369
Q

Investigations for cerebellar syndrome

A
  • Routine bloods: FBC, U&E, LFT, TFT, ESR/CRP, cholesterol, glucose
  • Other bloods: vitamin B12/E/folate, gluten serology, copper/caeruloplasmin, autoimmune screen, anti-GAD, paraneoplastic antibodies
  • MRI/CT brain
  • EEG
  • EMG
  • LP
370
Q

Complications of cerebellar syndrome

A
  • Respiratory arrest
  • Hydrocephalus
  • Tonic seizures
371
Q

What is meningitis?

A

Inflammation of the leptomeninges (arachnoid and pia mater)

372
Q

Causes of meningism

A

V - subarachnoid haemorrhage
I - bacterial, viral, fungal and parasitic
T - head injury
A - SLE
I - intrathecal drugs
N - paraneoplastic, malignancy
O - raised intracranial pressure

373
Q

Viral causes of meningitis

A
  • Enteroviruses: coxsackievirus, echovirus
  • Herpes simplex
  • Human immunodeficiency
  • Varicella zoster
  • Epstein Barr
  • Mumps
374
Q

Fungal causes of meningitis

A
  • Cryptococcus neoformans
  • Candida albicans
375
Q

Parasitic causes of meningitis

A

P. fallicidum

376
Q

How does infection spread to the brain in meningitis?

A
  • Direct - nose, anatomical defect (spina bifida, skull fracture), shunt, head operation, trauma, overlying skin
  • Bloodstream
377
Q

What is a risk factor for recurrent bacterial infection, often by pneumococcus?

A

Skull fracture (access to subarachnoid space)

378
Q

Causes of chronic meningitis

A
  • TB
  • Cryptococcus
  • Syphilis
  • Sarcoidosis
  • Behcet’s
379
Q

Risk factors for meningitis

A
  • Immunocompromised
  • Head operation
  • Trauma
  • Students (crowded environment)
  • Travel
  • Contact with someone with meningitis/TB
  • HIV
  • Spina bifida
  • Skull fracture
380
Q

What increases your risk of infection with Leptospira?

A

Working in drains, canals or polluted water, or recreational swimming

381
Q

Meningism triad

A
  1. Headache
  2. Neck stiffness
  3. Fever
382
Q

Symptoms of meningitis

A
  • Headache
  • Neck stiffness
  • Fever
  • Photophobia
  • Vomiting
  • Irritable
383
Q

Signs of meningitis

A
  • Kernig’s sign
  • Brudzinski’s sign
  • Reduced ROM in neck flexion
  • Temperature
  • In acute bacterial: petechial/purpuric non-blanching rash, seizures
384
Q

Signs of complications in meningitis

A
  • Progressive drowsiness
  • Lateralising signs
  • Cranial nerve lesions
385
Q

Investigations in meningitis

A
  • CT head
  • Lumbar puncture (contraindications: abnormal clotting (coagulation screen), petechial rash, raised intracranial pressure): microscopy, gram stain, Ziehl-Neelson stain, Indian ink, chocolate agar, PCR
  • Nose and throat swabs: chocolate agar, PCR
  • Stool PCR
  • Blood culture and PCR
  • Syphilis serology
386
Q

Gram +ve diplococci

A

S. pneumoniae

387
Q

Gram -ve diplococci

A

N. meningitidis

388
Q

Acid-fast bacilli

A

Tuberculosis

389
Q

Indian ink

A

Fungus

390
Q

Chocolate agar

A

H. influenzae
N. meningitidis

391
Q

Appearance of CSF (normal, bacterial, viral and fungal/TB)

A

N - clear
B - cloudy
V - clear
F - clear (cloudy fibrin web)

392
Q

Opening pressure of CSF (normal, bacterial, viral and fungal/TB)

A

N - 90-180
B - elevated
V - normal
F - normal-elevated

393
Q

WBCs of CSF (normal, bacterial, viral and fungal/TB)

A

N - <8
B - >1000
V - <300
F - <500

394
Q

Main cell type of CSF (normal, bacterial, viral and fungal/TB)

A

B - neutrophils
V - lymphocytes
F - lymphocytes

395
Q

Protein of CSF (normal, bacterial, viral and fungal/TB)

A

N - 15-45
B - >200
V - <200
F - >200

396
Q

Glucose of CSF (normal, bacterial, viral and fungal/TB)

A

N - 50-80
B - <40
V - normal
F - low-normal

397
Q

What extra investigations would you do for chronic meningitis?

A
  • MRI brain
  • Repeated CSF investigations
398
Q

Management of viral meningitis

A

Acyclovir if HSV/VZV
Conservative management for others

399
Q

Management of tuberculous meningitis

A
  • Antituberculosis drugs for at least 9 months: rifampicin, isoniazid, pyrazinamide
  • Adjuvant corticosteroids for 3 weeks, e.g. prednisolone
400
Q

Management of malignant meningitis

A

Intrathecal cytotoxic agents

401
Q

Complications of meningitis

A
  • Neuro - brain abscess, cerebral oedema, hydrocephalus, brain herniation, seizures, hearing loss, memory loss, cerebral palsy
  • Sepsis
402
Q

Prognosis of viral vs tuberculous vs bacterial meningitis

A

Viral generally self-limiting
Tuberculous 60% mortality
Bacterial 5% mortality when treated

403
Q

What is acute bacterial meningitis?

A

Serious bacterial infection of the meninges

404
Q

What organisms commonly cause bacterial meningitis in neonates?

A
  • Group B streptococcus (gram +ve cocci)
  • E. coli (gram -ve bacillus)
  • Listeria monocytogenes (gram +ve bacillus)
  • S. agalactiae
405
Q

What organisms commonly cause bacterial meningitis in children?

A
  • N. meningitidis (gram -ve diplococci)
  • S. pneumoniae (gram +ve diplococci)
  • H. influenzae B (gram -ve bacillus)
406
Q

What organisms commonly cause bacterial meningitis in adults?

A
  • S. pneumoniae (gram +ve diplococci)
  • N. meningitidis (gram -ve diplococci)
407
Q

What organisms commonly cause bacterial meningitis in immunocompromised?

A
  • Listeria monocytogenes (gram +ve bacillus)
  • M. tuberculosis (acid -fast bacillus)
408
Q

Other bacterial causes of meningitis

A
  • S. aureus
  • Treponema pallidum (syphilis)
  • Leptospira
409
Q

Why do cranial nerve palsies and hydrocephalus occur in acute bacterial meningitis?

A

Pia-arachnoid mater congested with poly,orphs and a layer of pus forms, which may organise to form adhesions

410
Q

Clinical manifestation of acute bacterial meningitis

A

Develops within minutes to hours
* Headache
* Neck stiffness
* Fever
* Photophobia
* Vomiting
* Intense malaise
* Rigors
* Irritable
* Prefers to lie still
* Positive Kernig’s sign
* Positive Brudzinski sign
* Seizures

411
Q

Signs of meningitis in babies

A
  • Hypotonia
  • Poor feeding
  • Lethargy
  • Hypothermia
  • Bulging fontanelle
412
Q

Clinical manifestation of meningococcal septicaemia

A
  • Petechial/purpuric non-blanching rash
  • Septic shock
  • Peripheral vascular infarcts
413
Q

Management of acute bacterial meningitis

A
  • IV antibiotics for at least 5 days
  • High-dose IV corticosteroid (dexamethasone) with or before dirst dose of antibiotics for 4 days
414
Q

Empirical antibiotic < 3 months, and alternative

A

Cefotaxime + amoxicillin
Benzylpenicillin + chloramphenicol

415
Q

Empirical antibiotics 3 months - 50 years, and alternative

A

Ceftriaxone
Benzylpenicillin + chloramphenicol

416
Q

Empirical antibiotics > 50 or immunocompromised, and alternative

A

Cefotaxime + ampicillin
Cefotaxime + co-trimoxazole

417
Q

Antibiotics for meningococcal infection

A

Cefotaxime initially
Benzylpenicillin if confirmed sensitivity

418
Q

Antibiotics for pneumococcal infection, and alternative

A

Cefotaxime
Penicillin

419
Q

Antibiotics for haemophilus infection, and alternative

A

Cefotaxime
Chloramphenicol

420
Q

Antibiotics for Listeria monocytogenes infection

A

Amoxicillin + gentamicin

421
Q

When should you add vancomycin in antibiotic treatment of meningitis?

A

Repeated abx use or foreign travel

422
Q

What abx therapy should you offer if penicillin and cephalosporin allergy?

A

Chloramphenicol

423
Q

Prophylaxis of bacterial meningitis

A
  • Notify public health
  • Antibiotic prophylaxis
  • Vaccines: meningococcal, Hib, pneumococcal
424
Q

What is the abx prophylaxis for meningitis?

A

Ciprofloxacin, rifampicin

425
Q

Who gets abx prophylaxis for meningitis?

A

Prolonged close contact during 7 days before onset and exposure to respiratory droplets

426
Q

Who gets meningococcal vaccine?

A
  • MenC and MenB in infancy and during outbreaks
  • Combined A and C meningococcal vaccine sometimes before travel to endemic regions (Africa, Asia)
  • MenC for close contacts if partially/un-immunised
427
Q

What is a complication of meningitis caused by N. meningitidis?

A

Waterhouse-Friedrichsen syndrome (adrenal gland failure due to bleeding into adrenal gland)

428
Q

Permanent effects of acute bacterial meningitis

A
  • Scars
  • Amputation
  • Hearing loss
  • Seizures
  • Brain damage
429
Q

What is narcolepsy?

A

Long-term brain condition that can prevent a person from choosing when to wake or sleep

430
Q

What causes narcolepsy?

A

Lack of brain chemical hypocretin (orexin), which regulates wakefulness
Thought to be autoimmune

431
Q

Which proteins are associated with narcolepsy?

A

HLA-DR2 and HLA-DQBI0602

432
Q

Possible triggers of narcolepsy

A
  • Hormonal changes: puberty, menopause
  • Major psychological stress
  • Infection or vaccination
433
Q

Clinical manifestation of narcolepsy

A
  • Excessive daytime sleepiness
  • Sleep attacks
  • Cataplexy (loss of muscle tone)
  • Sleep paralysis (inability to move or speak)
  • Excessive dreaming (as falling asleep or during waking) and waking in the night
434
Q

Investigations for narcolepsy

A
  • Sleep latency testing (rapid transition from wakefulness to sleep)
  • HLA testing
435
Q

Management of narcolepsy

A
  • Stop driving and inform DVLA
  • Good sleep hygiene
  • Modafinil dexamphetamine and methylphenidate (excessive daytime sleepiness)
  • Tricyclic antidepressants (clomipramine) or SSRIs (cataplexy)
436
Q

What is Meniere’s disease?

A

Long-term inner ear disorder that causes recurrent attacks of vertigo and symptoms of hearing loss, tinnitus and a feeling of fullness in the ear

437
Q

Cause of Meniere’s disease

A

Endolymphatic hydrops: excessive buildup of endolymph in the labyrinth of the inner ear, causing a higher pressure than normal and disrupting the sensory signals

438
Q

Risk factors for Meniere’s disease

A
  • Autoimmune diseases
  • Viral infections
  • Migraines
  • Trauma
  • Syphilis
  • Female
  • 40-50
439
Q

Clinical manifestation of Meniere’s disease

A

UNILATERAL
* Hearing loss (fluctuates, associted with vertigo)
* Vertigo (20 minutes to several hours, in clusters over several weeks)
* Tinnitus

440
Q

How is Meniere’s disease diagnosed?

A

Clinically, by an ENT specialist
* 2 spontaneous episodes of vertigo lasting 20 minutes to 12 hours
* Fluctuating hearing, tinnitus and/or perception of aural fullness
* Hearing loss confirmed by audiometry to be sensorineural, low-mid frequency and of the affected ear
* Not better accounted for by an alternative vestibular diagnosis

441
Q

What investigations would you do to exclude other causes of vertigo, hearing loss and tinnitus?

A
  • Bloods: FBC, U&E, TFT, lipid profile, syphilis screen
  • Audiogram
  • Imaging
  • Special tests: bithermal caloric test, electrocochleography and vestibular-evoked myogenic potential
442
Q

What is the management of acute attacks in Meniere’s disease?

A
  • Bed rest and reassurance
  • Prochlorperazine
  • Antihistamine (cyclizine, cinnarizine, promethazine)

NB: use buccal, IM or IV if vomiting

443
Q

How to prevent attacks in Meniere’s disease

A
  • Avoid triggers (e.g. salt, caffeine, fatigue, stress, allergies, chocolate, alcohol)
  • Betahistine prophylaxis
  • Chemical labyrinthectomy with ototoxic drugs (e.g. gentamicin)
  • Surgical decompression of endolymphatic compartment of inner ear
444
Q

Does someone with Meniere’s disease need to inform DVLA?

A

DVLA advise all people with ‘liability to sudden and unprovoked or unprecipitated episodes of disabling dizziness’ to stop driving and inform the DVLA

445
Q
A
446
Q

What would NCS and EMG show for myopathy?

A

NCS normal
EMG abnormal

447
Q

What would an EMG show in myasthenia gravis?

A

Jitter: time between contractions of 2 muscle fibres varies

448
Q
A
449
Q
A
450
Q

What is an investigation you could do for MND?

A

Motor evoked potential

451
Q

What is transient loss of consciousness?

A

Spontaneous loss of consciousness with complete recovery

452
Q

Fits, faints and funny dos

Causes of blackouts and funny turns

A

V - syncope, arrhythmia, TIA
T - head injury
M - hypoglycaemia
O - non-epileptic seizure, epileptic seizure, panic attack, severe vertigo, narcolepsy, migraine, hydrocephalic attack

453
Q

How can you tell the difference between syncope and epileptic seizures?

A

Syncope
* Likely to be older with comorbidities and cardiac risk factors
* Triggered by exertion or standing
* Goes pale/clammy, palpitations/chest pain and goes dark
* Eyes close, go floppy and collapse
* Recover within seconds

Epileptic seizure
* Triggers include alcohol, sleep deprivation, illness and lights
* May have aura or no warning
* Eyes open, side of tongue bite, staring, posturing
* Lasts minutes, with slow recovery (hours to days), feeling onfused and drowsy

454
Q

How to tell the difference between epileptic and non-epileptic seizures

A

Epileptic:
* Triggers include alcohol, sleep deprivation, illness and lights
* Aura or no warning
* Eyes open, side of tongue bite, staring, posturing
* Lasts minutes, with a slow recovery (hours to days), feeling confused and drowsy

Non-epileptic:
* Tend to have a psychiatric history and social stressors
* Can be triggered by heightened emotion
* Thrashing violent movements, pelvic thrusting, back arching, eyes closed, tip of tongue bite, crying, distractible and waxing/waning
* Long (up to an hour), with an unusually rapid recovery

455
Q

What is an epileptic seizure?

A

Sudden, transient episode of abnormal and excessive, hyper-synchronous discharge of cerebral neurones causing symptoms or signs

456
Q

What is epilepsy?

A

Ongoing tendency to experience recurrent epileptic seizures

457
Q

Cause of epileptic seizures

A

Too much excitation or too little inhibition of clusters of neurones in the brain to bcome temporarily impaired and send out excitatory paroxysmal signals
Fast/long-lasting activation of excitatory NMDA receptors and dysfunctino inhibitory GABA receptors

458
Q

How do the causes of epileptic seizures vary with age?

A

Children/teenagers: genetic, perinatal and congenital disorders
Younger adults: trauma, drugs and alcohol
Older adults (> 60): vascular disease and mass lesions (neoplasms)

459
Q

Causes of epileptic seizures

A

V - stroke, arteriovenous malformation, cavernous haemangiomas
I - encephalitis, cerebral abscess, tuberculomas, meningitis, HIV, cerebral toxoplasmosis
T - TBI, depressed skull fracture, penetrating injury, intracranial haemorrhage
A - autoimmune antibody-mediated encephalitis
M - hypoglycaemia, hypocalcaemia, hyponatraemia, hypoxia (cerebral palsy)
I - brain surgery, antipsychotics, tricyclic antidepressants, lithium, lidocaine, ciclosporin, withdrawal of antiepileptics and benzodiazepines
N - brain tumour
C - neuronal migration defects
D - Alzheimer’s
O - primary generalised epilepsies (childhood absence epilepsy, juvenile myoclonic epilepsy), alcohol, cocaine, hippocampal sclerosis, genetic disorders

460
Q

What is the most common cause of epilepsy after the age of 60?

A

Stroke

461
Q

How can neurocysticercosis present and what causes it?

A

Epileptic seizures
Pork tapeworm in India and South America

462
Q

What fraction of people with cerebral palsy have epileptic seizures?

A

1 in 3

463
Q

What % of people who have had brain surgery will have seizures after?

A

17

464
Q

What is a common presenting feature of brain tumour?

A

Seizures

465
Q

How can alcohol cause seizures?

A
  • Chronic alcohol ues
  • Heavy bouts of drinking
  • Periods of withdrawal
  • Alcohol-induced hypoglycaemia and head injury
466
Q

Risk factors for epileptic seizures

A
  • FH of epilepsy or other neurological illness
  • Premature birth
  • Genetic conditions associated with epilepsy
467
Q

How are focal seizures categorised?

A
  • Aura - hallucination, deja vu, fear
  • Motor
  • Loss of awareness and responsiveness
468
Q

What is a Jacksonian seizure?

A

One limb jerking

469
Q

Clinical manifestation of temporal lobe focal seizure

A
  • Deja vu or jamais vu
  • Fear
  • Olfactory, gustatory or auditory hallucinations
  • Altered perception
  • Abdominal rising sensation
  • Nausea
  • Vertigo
470
Q

Clinical manifestation of frontal lobe focal seizure

A

Conjugate gaze deviates away from epileptic focus and head turns

471
Q

Clinical manifestation of occipital lobe focal seizure

A

Visual phenomena: zigzag lines, coloured scotomas

472
Q

Clinical manifestation of parietal lobe focal seizure

A

Tingling, pain, numbness, prickling sensation

473
Q

Clinical manifestation of focal seizure originating within motor cortex

A
  • Jerking typically on one side of the mouth or one hand, sometimes spreading to involve the entire side (Jacksonian march)
  • Todd’s paralysis (temporary paralysis of affected limbs)
474
Q

Clinical manifestation of focal seizure with altered awareness or responsiveness

A
  • Aura followed by period of complete or partial loss of awareness of surroundings, lasting for 1-2 minutes, which they don’t remember
  • Speech arrest
  • Automatisms, e.g. lip smacking, dystonic limb posturing, walking in circle, undressing, swallowing, chewing, finger movements
475
Q

What is the difference between focal and generalised seizures?

A

Focal on one hemisphere, generalised both hemispheres

476
Q

Clinical presentation of absence seizures

A
  • Begin in childhood (childhood/juvenile absence epilepsy)
  • Loss of awareness and vacant expression for < 10 seconds before returning abruptly to normal as though nothing happened
  • Slight fluttering of eyelids
477
Q

Clinical manifestation of tonic-clonic generalised seizure

A
  • Often no aura
  • Initial tonic stiffening followed by clonic synchronous jerking of the limbs, reducing in frequency over 2 minutes until the convulsions stop
  • Eyes remain open
  • May bite their tongue, be incontinent, breathe irregularly and utter an initial cry
  • Flaccid unresponsiveness followed by gradual return of awareness with confusion and drowsiness lasting 15 minutes to over an hour
478
Q

Clinical manifestation of myoclonic seizures

A
  • Momentary brief contractions of muscle(s)
  • Typically in teenagers (juvenile myoclonic epilepsy)
  • Often in morning after waking
  • Triggered by lack of sleep, alcohol, strobe lighting
479
Q

Clinical manifestion of tonic seizures

A

Stiffening of body and fall, usually backwards

480
Q

Clinical manifestation of atonic seizure

A

Sudden collapse with loss of muscle tone, falling forwards

481
Q

Clinical manifestation of clonic seizure

A

Violent muscle contractions, jerking of limbs and trunk which accelerate and decelerate

482
Q

Investigations for ?seizures

A
  • ECG (transient tachyarrhythmias)
  • MRI brain in those with focal seizures and older patients where there’s a greater chance of focal brain lesions
  • Bloods: blood gas, U&E, glucose, ESR/CRP, Ca
  • Infection screen: urine culture, blood culture, LP
  • EEG (classification or epilepsy): sleep recordings, 24 hour ambulatory EEG, inpatient EEG videotelemetry
483
Q

What is hippocampal sclerosis?

A

Damage with scarring and atrophy of the hippocampus and surrounding cortex
Seizures

484
Q

EEG signs of absence seizure

A

3 Hz spike-and-wave

485
Q

Signs of primary generalised epilepsies on EEG

A

Focal cortical spikes or generalised spike-and-wave activity

486
Q

EEG activity during status epilepticus

A

Continuous activty

487
Q

What is EEG for?

A

Classification of epilepsy, not distinguishing epilepsy from other attacks (incidental abnormalities in 0.5% of healthy adults (higher proportion in people with learning disability or previous CNS insult) and high false-egative rates)

488
Q

Safety advice for people who have had a seizure

A
  • Avoid swimming and dangerous sports, e.g. rock climbing
  • Leave bathroom unlocked
  • Take showers, not baths
  • Have carpets and radiator covers
  • Microwave meals
  • Caution with heights, traffic and heavy equipment
  • Stop driving for 6 months after 1 seizure or withdrawing from AEDs, until seizure-free for 12 months if recurrent seizures (5 years before 70 year driving license)
489
Q

Drugs for epilepsy

A

When firm clinical diagnosis of epilepsy with risk of recurrent seizures, consider AEDs:
* Introduce at low dose and slowly titrate upwards until seizure-free or maximum tolerated dose
* If not seizure-free, introduce second AED and slowly withdraw first
* If still not seizure-free, try combination therapy

490
Q

If seizures are not controlled with multiple drugs, what do you do?

A
  • Check concordance
  • Serum AED level
  • Review diagnosis
491
Q

AEDs for generalised tonic clonic seizures

A
  • Levetiracetam
  • Sodium valproate
  • Lamotrigine
492
Q

AEDs for focal seizures

A
  • Levetiracetam
  • Carbamazepine
  • Lamotrigine
493
Q

AEDs for absence seizures

A
  • Ethosuximide
  • Valproic acid
  • Lamotrigine
494
Q

AEDs for myoconic seizures

A
  • Levetiracetam
  • Sodium valproate

NOT carbamazepine

495
Q

Management of epilepsy where drugs don’t work

A
  • Resective epilepsy surgery (focal structural abnormality), e.g. temporal lobectomy (hippocampal sclerosis)
  • Vagal nerve stimulation
  • Ketogenic diet
496
Q

When can you consider withdrawing AEDs?

A

Seizure-free for 2 years
(50% have another seizure)

497
Q

Initial management of seizure

A
  • Place in safe position
  • Airway
  • High concentration oxygen
  • IV access
  • Prepare emergency medication
  • Blood glucose
  • If hypoglycaemic 150-200ml 10% glucose stat and commence 10% glucose infusion at 100ml/hour if seizures continue
  • If alcohol excess/malnutrition 1 pair Pabrinex IV before glucose replacement
498
Q

Management of seizure at 5-15 minutes

A

Benzodiazepine, wait 5 minutes, 2nd dose
* IV lorazepam 4mg bolus
* Buccal midazolam 10mg
* Rectal diazepam

499
Q

Management of seizures after 2 doses of benzodiazepine

A
  • Inform anaesthetic team and ITU
  • Dose 3: IV phenytoin (ECG monitoring!), valproate or levetiracetam
  • Following complete infusion, consider 2nd IV AED infusion of a different drug or IV phenobarbital
  • General anaesthesia with intubation and ventilation: propofol, repeat bolus, followed by continuou infusion
500
Q

Care after seizure

A
  • ABCDE at regular intervals
  • Consider critical care
  • Reinstate previous AED via NG tube
  • Look for underlying cause (CT/MRI head)
  • Review management of epilepsy
501
Q

Complications of epilepsy

A
  • Todd’s paralysis (paralysis of limbs afected, subsides after 2 days)
  • Status epilepticus
  • Sudden unexplained death in epilepsy
  • Recurrent seizures (75%)
502
Q

Side effects of AEDs

A
  • Unsteadiness
  • Nystagmus
  • Drowsiness
  • Significant cognitive side effects
  • Skin rash
  • Blood dyscrasias
503
Q

What is status epilepticus?

A

A seizure lasting more than 5 minutes, or 2 or more seizures without regaining consciousness in the interim

504
Q

What % of status epilepticus have epilepsy?

A

50

505
Q

Presentation of status epilepticus

A

Sustained generalised tonic clonic seizure which eventually becomes little movements (e.g. twitching around eye) or long absence/impaired awareness (altered mental state, subtle twitching, unusual behaviour)

506
Q

What % of status epilepticus are non-epileptic seizures?

A

25%

507
Q

Complications of status epilepticus

A
  • Death
  • Permanent cerebral damage: epilepsy, focal neurological deficits, encephalopathy
  • Severe hypoxaemia > end organ damage
  • Rhabdomyolysis > AKI
  • Hyperthermia
  • Cardiac arrhythmias
  • Metabolic acidosis
  • Shock
  • Cerebral oedema
508
Q

What is a non-epileptic seizure?

A

Episodes of change in movement, sensation or experience that resembles epileptic seizures, but without the cerebral discharges

509
Q

Risk factors for non-epileptic seizures

A
  • Psychiatric illness
  • Other somatoform disorders
  • Childhood sexual abuse
  • Female
  • Social/personal stressors
510
Q

Clues that a seizure may be non-epileptic

A
  • Long, up to an hour
  • Unusually rapid recovery
  • Situational, when heightened emotion
  • Eyes closed
  • Thrashing violent movements
  • Crying
  • Pelvic thrusting
  • Back arching
  • Tip of tongue bite
  • Waxing and waning symptoms
  • Distractible
  • No cyanosis or incontinence
511
Q

Is oxygen affected in non-epileptic seizures?

A

No

512
Q

Management of non-epileptic seizures

A
  • Reassure
  • Psychiatric referral
  • Avoid AEDs and benzodiazepines
  • Support groups and online resources
513
Q

What is a febrile convulsion?

A

Seizure that occurs in children with a high fever

514
Q

Difference between simple and complex febrile convulsion

A

Simple - generalised tonic clonic seizure lasting less than 15 minutes and only occurring once during a single febrile illness
Complex - partial or focal seizures lasting more than 15 minutes or occurring multiple times during the same febrile illness

515
Q

Typical presentation of febrile convulsions

A

Child around 18 months presents with 2-5 minute tonic clonic seizure during high fever, usually caused by an underlying infection, e.g. tonsilitis

516
Q

Management of febrile convulsion

A
  • Identify and manage source of infection
  • Control fever with simple analgesia (paracetamol, ibuprofen)
  • Safety net: stay with child, put them in safe place (carpeted floor with pillow under head), call ambulance if lasting more than 5 minutes
517
Q

What is Guillain-Barre syndrome?

A

Autoimmune, rapidly progressive demyelinating condition of the peripheral nervous system, often triggered by an infection

518
Q

What are the different types of GBS?

A
  • Acute inflammatory demyelinating polyneuropathy (90%)
  • Acute motor axonal neuropathy
  • Acute motor and sensory axonal neuropathy
  • Miller-Fisher syndrome
519
Q

What causes GBS?

A

Infection
Molecular mimicry: pathogenic antigen and myelin gangliosides in PNS share homologous epitopes, so the pathogen induces an antibody response (anti-ganglioside antibodies) against the myelin sheath of sensory and motor nerves, causing demyelination in patches along the length of the axon (segmental demyelination)

520
Q

Risk factors for GBS

A
  • Male
  • 15-35 or 50-75
  • GI or respiratory tract infection
  • Lymphoma
  • Influenza vaccine
521
Q

What are the most common organisms of infection that trigger GBS?

A

Bacterial: campylobacter jejuni, mycoplasma pneumoniae
Viral: CMV, influenza, EBV, zika virus

522
Q

Clinical manifestation of GBS

A
  • Infection 1-2 weeks prior
  • Lower back and leg pain
  • Symmetrical paralysis and/or acroparaesthesia (tingling, numbness, etc.) affecting the distal limbs first (legs) and progressing proximally over several days to 6 weeks (upwards)
  • Loss of tendon reflexes in affected limbs
  • May progress to respiratory muscle weakness (SOB)
  • Cranial nerve involvement: speech problems, diplopia, facial droop
  • Autonomic dysfunction: tachycardia, HTN, postural hypotension, urinary retention
523
Q

Clinical manifestation of Miller-Fisher syndrome

A

Ocular muscle palsies and ataxia

524
Q

What criteria diagnoses GBS?

A

Brighton criteria

525
Q

What criteria is in the Brighton criteria?

A
  • Symmetric flaccid limb weakness
  • Lack or absent deep tendon reflexes in limbs with weakness
  • Monophasic course and time between appearance of signs from 12 hours to 28 days
  • CSF cellularity < 50 /uL (normal)
  • CSF protein concentration greater than normal (1-3 g/L)
  • Nerve conductino studies consistent with subtype of GBS
  • Lack of an alternative diagnosis for weakness
526
Q

What would nerve conduction studies show in GBS?

A

Abnormal in 85%
Slowing of conduction, prolonged distal motor latency and/or conduction block

527
Q

What must you screen for before starting Ig therapy in GBS and why?

A

IgA deficiency
Severe allergic reactions due to IgG antibodies if congenital IgA deficiency

528
Q

What investigations are needed to diagnose GBS?

A
  • Lumbar puncture
  • Nerve conduction studies
529
Q

What antibodies are involved in GBS?

A

Anti-ganglioside antibodies

530
Q

What imaging for GBS?

A

MRI brain and spinal cord

531
Q

Treatment of GBS

A
  • IV immunoglobulin for 5 days within the first 2 weeks
  • Repeat IV Ig if low and stable but not improving after 2 weeks
    OR
  • Plasma exchange
532
Q

Major complication of GBS and management

A

Ventilatory failure
Admit to ITU if signs of bulbar dysfunction or respiratory depression
Mechanical ventilation

533
Q

What prophylaxis needs to be considered in GBS?

A

Thromboprophylaxis with LMWH and compression stockings

534
Q

What is it important to monitor in someone with GBS?

A

Vital capacity, if maximal expiratory pressure reduced by more than 30% go to ITU as emerging respiratory muscle weakness and may need mechanical ventilation

535
Q

Complications of GBS

A
  • Type 2 respiratory failure
  • Impaired mobility > venous thrombosis, PE
  • Intubation > respiratory tract infaction
  • Psychiatric: depression, PTSD, anxiety
536
Q

Prognosis of GBS

A

7% die
Prolonged recovery phase (months to years)
20% unable to walk unaided for 6 months
75% fully recover

537
Q
A
538
Q

What is anterior horn cell syndrome?

A

Disorders of the anterior grey matter horns of the spinal cord, presenting with flaccid weakness and areflexia

539
Q

Causes of anterior horn cell syndrome

A
  • Motor neurone disease
  • Spinal muscular atrophy
  • Poliomyelitis
  • Anterior spinal artery ischaemia
  • Hopkins syndrome (status asthmaticus)
540
Q
A
541
Q

How does carbamazepine work in epilepsy?

A

Inhibits sodium channels

542
Q
A

Phase 3a Medicine (7 decks)

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