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Neurology Flashcards

1
Q

Describe the basic components & functions of the CNS

A
  • Cerebral hemispheres
    • Higher functions, motor and sensory (conscious), emotion, memory
  • Brainstem, cerebellum
    • Communication via cranial nerves- functions such as eye movement, swallowing, cardiorespiratory homeostasis
    • Cerebellum involved with motor sequencing and co-ordination
  • Spinal cord
    • Ascending (sensory) and descending (motor) pathways
    • Spinal reflex arcs
    • Control of upper and lower limbs at level of cervical and lumbosacral enlargements
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2
Q

Differentiate between grey and white matter?

A
  • Grey matter
    • Cell bodies and dendrites
      • There are axons; the volume is mainly the cell bodies and dendrites
    • Very vascular
  • White matter
    • Axons with no cell bodies
    • Myelin is white and fatty
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3
Q

How many segments of the spinal cord?

A
  • 31 segments
  • Dermatome and myotome each side
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4
Q

Differentiate between: a sensory deficit in a dermatomal pattern, across multiple segments and in a homuncular pattern- where is the lesion?

A
  1. Sensory deficit in dermatomal pattern = lesion at level of dorsal roots or spinal nerves
  2. Sensory deficit across multiple segments = cord lesion
  3. Sensory deficit in homuncular pattern = lesion above thalamus
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5
Q

Differentiate between a funiculus, a tract and a fasciculus?

A
  • Funiculus- large segment of white matter containing multiple distinct tracts in both ascending + descending direction
  • Tract- anatomically + functionally defined white matter pathway connecting 2 distinct regions of grey matter
  • Fasciculus- subdivision of a tract supplying a distinct body region
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6
Q

What is a nucleus?

A
  • A collection of functionally related cell bodies in the CNS
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7
Q

What is a ganglion?

A
  • A collection of functionally related cell bodies outside the CNS
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8
Q

Describe the arrangement of grey and white matter of the spinal cord and of the brain?

A
  • Spinal cord: grey matter centrally + white matter outer shell
  • Cerebrum: outer grey matter and inner white matter
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9
Q

Describe the different parts of the brainstem?

A
  • Midbrain (mesencephalon)- eye movements and reflex responses to sound and vision
  • Pons- feeding and sleeping
  • Medulla- cardiovascular + respiratory centres, contains major motor pathway- pyramids
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10
Q

Difference between gyrus and sulcus?

A
  • Gyrus is a raised fold of cerebral cortex
  • Sulcus is the valley between adjacent gyri
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11
Q

What does the central sulcus separate?

A
  • Precentral (motor, anterior) and postcentral (sensory, posterior) gyri
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12
Q

How is cerebrospinal fluid produced?

A
  • Ventricles contain choroid plexus- highly vascular- makes 600-700ml CSF a day
  • Path of CSF:
    • 2 lateral ventricles (most CSF is made here)
    • Interventricular foramen
    • Third ventricle (squashed flat in the midline by thalamus either side)
    • Cerebral aqueduct (within midbrain, common site of blockage)
    • Forth ventricle (sits beneath cerebellum)
    • Medial aperture (foramen of magenda)
      Lateral aperture (foramen of Luschka)
      Central canal to spinal cord
    • Subarachnoid space, bathing external surface of brain
    • Circulation via granulations
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13
Q

Functions of the CSF?

A
  • Protection- cushion for brain
  • Buoyancy- reduces net weight of brain à reduces pressure on base of brain
  • Chemical stability- K
  • Lots of glucose- nourishes
  • Immune function
  • Clearing waste products produced by brain cells
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14
Q

What happens if the ventricular system is blocked?

A
  • Blockage of a part of the ventricular system will lead to upstream dilatation
  • Commonest site for blockage- cerebral aqueduct- due to congenital stenosis or tumour
    • à dilatation of lateral + third ventricles but normal 4th
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15
Q

What sort of neurological symptoms do you ask about during a systems review?

A
  • General: fits, falls, LoC, headache, dizziness, vision/ hearing, memory loss, neck stiffness/ photophobia
  • Motor: weakness/ wasting, incontinence
  • Sensory: pain, numbness, tingling
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16
Q

What are some red flags for headache?

A
  • Intracranial bleed- thunderclap headache, recent trauma
  • Raised ICP- posture or Valsalva related
  • SoL- immunosuppression, malignancy, focal neurology, onset > 50 yrs
  • Meningitis- rash, fever, neck stiffness, photophobia
  • Temporal arteritis- visual problems, jaw claudication, scalp tenderness
  • Glaucoma- visual blurring, red eyes, halos
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17
Q

List some clinical circumstances in which CSF examination may be helpful?

A
  • Suspected subarachnoid haemorrhage
  • Suspected meningitis/ encephalitis
  • Immunological disorders- MS, GBS
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18
Q

Compare the typical CSF findings in bacterial, viral and tuberculous meningitis to normal CSF results

A

Appearance

Opening pressure

WBC

Glucose

Protein

Normal

Clear and colourless

10-20 cm H2O

0-5 cells/uL

No neutrophils, primarily lymphocytes

  1. 8-4.2 mmol/L or >60% of plasma glucose conc.
  2. 15-0.45 g/L or <1% of serum protein conc.
    * Bacterial meningitis*

Cloudy and turbid

↑ (>25 cm H2O)

↑ >100 cell/uL

Low (<40% of serum glucose)

↑ (> 50 mg/dL)

Viral meningitis

Clear

Normal or ↑

↑ (50-1000 cells/uL, primarily lymphocytes)

Normal (>60% of serum glucose)

↑ (>50 mg/dL)

Tuberculous/ fungal

Clear or cloudy

↑

↑ (10-500 cells/ uL)

Low

↑

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19
Q

Describe the typical CSF findings in subarachnoid haemorrhage

A
  • Appearance: blood-stained initially, then xanthochromia (yellowish) >12 hours later
  • Opening pressure: ↑
  • WBC: ↑
  • RBC: ↑
  • Glucose: normal
  • Protein: ↑
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20
Q

Describe the typical CSF findings in Guillain-Barre syndrome

A
  • Appearance: clear or xanthochromia
  • Opening pressure: normal or ↑
  • WBC: normal
  • Glucose: normal
  • Protein: ↑
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21
Q

How many patients develop a headache following lumbar puncture? Who is most at risk and why do they occur?

A
  • Approximately 1/3
  • Pathophysiology is unclear but may relate to a leak of CSF following dural puncture
  • More common in young females with a low BMI
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22
Q

What are some contraindications to lumbar puncture?

A
  • Signs suggesting raised intracranial pressure or reduced or fluctuating level of
  • Consciousness (glasgow coma scale score less than 9 or a drop of 3 points or more)
  • Relative bradycardia and hypertension
  • Focal neurological signs
  • Abnormal posture or posturing
  • Unequal, dilated or poorly responsive pupils
  • Papilloedema
  • Abnormal ‘doll’s eye’ movements
  • Shock
  • Extensive or spreading purpura
  • After convulsions until stabilised
  • Coagulation abnormalities or coagulation results outside the normal range or platelet
  • Count below 100x109/litre or receiving anticoagulant therapy
  • Local superficial infection at the lumbar puncture site
  • Respiratory insufficiency in children
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23
Q

Describe features of a post lumbar puncture headache

A
  • Usually within 24-48 hrs following LP
    • But can be up to 1 week later
  • May last several days
  • Worsens with upright position
  • Improves with recumbent position
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24
Q

What factors can contribute to developing a post LP headache?

A
  • Increased needle size
  • Direction of bevel
  • Increased number of LP attempts
  • Not replacing the stylet
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25
Q

How is a post-lumbar puncture headache treated?

A
  • Supportive- analgesia, rest
  • If pain continues for > 72 hours then specific treatment is indicated to prevent subdural haematoma
  • Treatment options include: blood patch, epidural saline, IV caffeine
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26
Q

Define a seizure and define epilepsy?

A
  • A seizure is a transient occurrence of signs + symptoms due to abnormal excessive or synchronous neuronal activity in the brain
  • Epilepsy is the name for occasional sudden, excessive, rapid and local discharges of grey matter. It is a disease of the brain defined by any of the following:
    • At least 2 unprovoked seizures > 24 hrs apart
    • 1 unprovoked seizure and a probability for further seizures similar to the general recurrence risk after 2 unprovoked seizures, occurring over the next 10yrs
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27
Q

What are some causes of epilepsy?

A
  1. Genetic
  2. Structural- eg chronic cerebrovascular disease, congenital malformation
  3. Metabolic disorder
  4. Immune disorder
  5. Chronic infection eg HIV
    (acute infection- meningitis)
  6. Unknown (1/3 pts)
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28
Q

Describe the pathophysiology of epilepsy?

A
  • Seizures occur due to an imbalance between excitatory and inhibitory signals in the brain
  • High-frequency bursts of excitatory action potentials in neurones- synchronous, hyperexcitable activity within a neuronal population
  • GABA is the main inhibitory neurotransmitter, gabanergic neurones
  • Glutamate is the main excitatory receptor
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29
Q

List some risk factors for developing epilepsy?

A
  • Cerebrovascular disease
  • Head trauma
  • Cerebral infections
  • Fhx
  • Premature birth
  • Congenital malformations of the brain
  • Genetic conditions associated with epilepsy
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30
Q

How is a diagnosis of epilepsy made?

A
  • 1 of 3 criteria
  1. ≥2 unprovoked (or reflex) seizures occurring > 24 hrs apart
  2. 1 unprovoked (or reflex) seizure with a probability of further seizures felt to be a similar recurrence risk to pts with ≥2 unprovoked seizures over the next 10 years
  3. A diagnosed epilepsy syndrome
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31
Q

What are some differentials for epilepsy?

A
  • Syncope and anoxic seizures
  • Behavioural, psychological, psychiatric- pseudoseizures
  • Sleep-related conditions
  • Paroxysmal movement disorders
  • Migraine associated disorders
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32
Q

How would you investigate someone with suspected seizures?

A
  • ECG- exclude problems with the heart
  • Bloods- FBC, U&Es, LFT, glucose, bone profile
  • EEG (electroencephalogram)- assess and record electrical activity of brain
    • To support epilepsy diagnosis, assess recurrence risk, determine seizure type
  • MRI brain- to visualise the structure of the brain, assess any structural abnormalities that may be associated with the seizures
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33
Q

How are seizures classified?

A
  1. Where the seizures begin in the brain
    1. Focal, generalised, or focal to bilateral tonic clonic
  2. Level of awareness during a seizure
    1. Impaired awareness or normal awareness (complex or partial)
  3. Other features of seizures
    1. Motor or non-motor
      1. Absence, tonic-clonic, myoclonic, atonic, spasms
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34
Q

How to define where seizures begin?

A
  • Focal seizures (previously partial seizures), start in an area or network of cells on 1 side of brain
  • Generalised seizures: engage or involve networks on both sides of the brain at the onset
  • Unknown onset
  • Focal to bilateral seizure (previously secondary generalised): started in one side of the brain and spread to both sides
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35
Q

How to describe a patients awareness during a seizure?

A
  • Focal aware (previously simple partial): awareness remains intact, even if the pt is unable to talk or respond during the seizure
  • Focal impaired awareness (previously complex partial): awareness is impaired or affected at any point during seizure, even if the pt has a vague idea of what happened
  • Awareness unknown
  • Generalised seizures: presumed to affect pt’s awareness or consciousness in some way
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36
Q

How to describe motor and other symptoms in focal seizures?

A
  • Focal motor seizure: some type of movement occurs eg twitching, jerking, stiffening movements of a body part or automatisms (licking lips, rubbing hands, walking, running)
  • Focal non-motor seizure: other symptoms occur first such as changes in sensation, emotions, thinking, or experiences
  • Auras: early symptoms may be the start of a seizure
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37
Q

What are the different types of generalised seizure?

A
  • Generalised tonic-clonic seizures (grand mal)- most common type
    • Loss of consciousness
    • Tonic- muscle tensing
    • Clonic- muscle jerking
    • Other features- tongue biting, incontinence, groaning, irregular breathing
    • Pro-longed post-ictal period- confused, drowsy, irritable, depressed
  • Tonic
    • Pt becomes stiff + flexed
    • Pt can fall backwards
  • Clonic
    • `
    • 0
  • Typical absence (petit mal)
    • Typically occur in children
    • Pt becomes blank, stares into space, LoC, then abruptly returns to normal
    • Unaware of surroundings during episode + won’t respond
    • 10-20seconds
  • Atonic
    • Drop attacks
    • Brief lapses in muscle tone
    • <3 mins
    • Typically begin in childhood
  • Myoclonic
    • Myoclonus = shock-like contraction of a muscle or group of muscles
      • Myoclonus can occur in people w/o epilepsy eg when falling asleep or just occasionally during the day
    • In pts with myoclonic seizure, the jerks are more frequent, often during sleep or 1st thing in morning
    • May affect whole body or single limb
    • No aura, loss of awareness or post-ictal confusion
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38
Q

What are focal seizures and what are the different types of focal seizure?

A
  • Focal seizures begin in temporal lobe
  • Affect hearing, speech, memory, emotions
  • Features include hallucinations, memory flashbacks, déjà vu, doing strange things on autopilot

TYPES:

  • Focal aware
    • Pt is awake and aware during seizure even if they can’t talk or respond
  • Focal impaired awareness
    • Lasts 30 seconds- 2 mins
    • Pt is confused, awareness is affected
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39
Q

What are the commonest seizures in clinical practice?

A
  • Tonic-clonic
  • Absence
  • Focal impaired awareness (complex partial)
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40
Q

Describe what happens during a generalised tonic-clonic seizure?

A
  • Tonic activity
    • Loss of consciousness when seizure begins, pt may fall
    • Strong tonic spasms of the muscles can force air out of lungs- cry or moan may be heard
    • Saliva or foam may come out of mouth, tongue, oral mucosa bites with blood in saliva
    • Stiffness of the chest muscles may impair breathing- cyanosis- pts face may look blue, may gasp or gurgle
  • Clonic activity
    • Jerking movements affect the face, arms and legs, becoming intense and rapid
    • After 1-3 mins, the jerking movements slow down and the body relaxes including the bowel or bladder
    • Pt may let out deep sigh or return to normal breathing
  • Post-ictal period
    • May remain unconscious for several mins as brain recovers
    • Gradually regain awareness, may feel confused, exhausted, sore, sad, embarrassed
    • Post-ictal amnesia
    • May have abnormal or combative or even psychotic
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41
Q

List some causes of seizures

A
  • Cerebral tumours
  • Intracranial infection
  • Head injury
  • Illicit drugs
  • Alcohol
  • Hypoxia
  • Stroke
  • Electrolytes
    • Low Na
    • Low Ca
    • Low Mg
    • Hypoglycaemia
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42
Q

What are the types of epilepsy?

A
  • Focal epilepsy: any focal seizure types
  • Generalised epilepsy: generalised seizure types
  • Generalised and focal epilepsy: combination
  • Unknown epilepsy: insufficient evidence to conclude which type of epilepsy it is
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43
Q

What is an epilepsy syndrome, what are the types, and how is it diagnosed?

A
  • Epilepsy may be organised into a specific syndrome
  • Characterised by recurrent propensity to a specific seizure type or types of seizures
  • Important to determine a syndrome to guide medical therapy with anti-epileptic drugs (AEDs)
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44
Q

What is primary generalised epilepsy?

A
  • There is a strong underlying genetic basis
  • 3 seizure types occur to varying degrees- myoclonus, generalised tonic clonic seizures and absence seizures
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45
Q

What are some examples of classic epilepsy syndromes?

A
  • West syndrome
  • Lennox Gastaut syndrome
  • Juvenile myoclonic epilepsy
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46
Q

List 5 causes of secondary epilepsy.

A
  1. Stroke
  2. SoL
  3. Severe head injury
  4. Drug abuse or alcohol misuse
  5. Brain infection
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47
Q

Child presents with seizures, what do you need to do in AMU?

A
  • PMH
    • Gestational
    • Birth
    • Developmental milestones
    • Schooling
    • Head injury
  • Drugs history
    • Opioids
    • Alcohol
    • Illicit drugs
  • FHx of epilepsy
  • Clinical assessment
    • General full examination
    • Full neuro examination
      • GCS/ MOCA
      • Cranial nerves
      • Power, tone, reflexes
      • Funduscopic
    • Ix
      • Bloods- FBC, U&Es, LFTs, CRP, calcium, Mg, PO4, glucose
      • Glucose
      • ECG
      • Urine dip
      • Neuro obs, normal obs including temperature.
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48
Q

How to manage epilepsy holistically?

A
  • Stop driving, inform DVLA
  • Inform occ health at work
  • Safety advice- no swimming, heights, occupation
  • Contact GP if further seizures
  • OP MRI and baseline EEG
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49
Q

How to manage a patient who is actively seizing in front of you?

A
  • ABCDE
    • Protect airway, recovery position
    • Give high flow O2
    • Fluids
    • BM-10% or 50% glucose if low
      • Hypoglycaemia is one of the commonest reversible causes of seizures, so always check blood glucose level and correct
    • ECG
    • U&Es, glucose, Ca, Mg, LFTs, FBC
    • Anticonvulsant levels, tox screen
  • Seizures > 5 mins
    • Lorazepam, IV 4mg bolus, repeat once after 10 mins if seizures continuing
    • If seizure continues- start preparing phenytoin
  • Establishes status > 25 mins
    • Phenytoin 20mg/kg over 20mins
    • IV valproate, levetiracetam
      • Take advice from neurologist
      • Alert ITU
  • Refractory status > 30 mins
    • General anaesthesia, high dose propofol
    • Continue for 12-24 hrs after last clinical or EEG seizure, then wean sedation
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50
Q

What are the major complications of epilepsy?

A
  • Status epilepticus
  • Sudden unexpected death in epilepsy (SUDEP)
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51
Q

What are some risk factors for Sudden Unexpected Death in Epilepsy (SUDEP)?

A
  • Uncontrolled or frequent seizures
  • Generalised tonic-clonic seizures
  • Seizures begin at young age, many years of living with epilepsy
  • Missed doses of medicine
  • Alcohol
  • Nocturnal seizures
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52
Q

What are the regulations with regard to driving for people who have been diagnosed with epilepsy?

A
  • First seizure- do not drive for 6 months, reapply if no seizure
  • Epilepsy- do not drive for 12 months, reapply if no seizure
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53
Q

Define status epilepticus?

A
  • A single seizure lasting > 5 minutes
  • Or more than or equal to 2 seizures within a 5 minute period w/o the person returning to normal between them
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54
Q

Causes of Status Epilepticus

A
  • Pre-existing diagnosis of epilepsy:
    • AED withdrawal
    • Non-compliance
    • Alcohol use + withdrawal
    • Illicit drugs
    • Intercurrent infection
    • Progression of underlying disease- tumour, encephalitis, vasculitis
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55
Q

Describe how to manage status epilepticus?

A
  • ABC
    • Airway adjunct
    • O2
    • Check blood glucose
  • First-line drugs benzodiazenes- diazepam, lorazepam
    • Pre-hospital setting rectal diazepam
    • Hospital setting IV lorazepam
      • Can be repeated once after 10-20 minutes
  • If on going or established status start second line drug such as phenytoin or phenobarbital infusion
  • If no response (refractory status) within 45 mins from onset, best way to rapidly achieve control is induce a general anaesthetic
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56
Q

What sort of things should you include in a history for a headache?

A
  • Mode of onset
  • Duration
  • Nature of headache- sharp, dull, throbbing
  • Site of headache- localised, variable, generalised
  • Pattern & timing- including time of day, relation to menstruation
  • Provoking & relieving factors- coughing, posture
  • Associated symptoms- aura
  • Drug hx- analgesics
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57
Q

What is meant by the terms primary and secondary headache?

A
  • Primary headache- migraine, tension type headache, cluster headaches and other rarer trigemino-autonomic cephalgia
  • Secondary headache- caused by a separate underlying pathological process that may be amenable to treatment
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58
Q

List some causes of a secondary headache

A
  • Vascular
  • Haemorrhage
  • Infective
  • Neoplastic
  • Drugs
  • Inflammation
  • Raised ICP
  • Trauma
  • Metabolic
  • Toxins
  • Glaucoma
  • Sinus disease
  • Hypertension
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59
Q

What are some red flags for headaches?

A
  • Thunderclap headache
    • Sudden means vascular until proven otherwise
    • SAH is the first differential
  • Meningism- neck stiffness & photophobia
    • Meningitis
    • Blood in subarachnoid space
  • Non-blanching purpuric rash (doesn’t blanch due to bleeding into the tissues)
    • Meningococcal septicaemia
  • Fever
    • Intracranial infection- meningitis, encephalitis
    • Viral infection
  • Focal neurology
    • Serious causes consider infection, vascular, inflammation, SoL, severely raised ICP
  • Features of raised ICP- headache present on waking & worse lying down, possible N&V, CSF pressure is increased in supine pressure, may be associated confusion, cognitive slowing, diplopia, papilloedema, other focal signs
  • Exacerbation by valsalvala/ bending/ cough
    • Raised ICP
    • Chiari malformation
  • Recent onset or change in character
    • Secondary causes
  • Previous malignancy
    • Mets?
  • Constitutional symptoms- malaise, night sweats, wt loss, jaw claudication, scalp tenderness, headache over temple, tenderness or redness or swelling over temporal artery, over age 50
    • Temporal arteritis
  • New onset headache in older pt
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60
Q

What is the Glasgow coma scale used for & how is it performed?

A
  • Initially designed for use in head injury, now used to measure consciousness
  • Score 3-15
  • Motor 6- (1) no response to pain, (2) extensor posturing to pain (3) abnormal flexor response to pain (4) withdraws to pain (5) localising response to pain (6) obeying command
  • Verbal 5- (1) no response (2) incomprehensible speech- moaning but no words (3) inappropriate speech- random words (4) confused conversation (5) oriented
  • Eye opening 4- (1) no eye opening (2) opening to response to pain to limbs (3) open in response to speech (4) spontaneous eye opening
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61
Q

Describe the clinical features for migraine

A
  • Severe unilateral throbbing headache
  • Associated with nausea, photophobia and phonophobia
  • Attacks may be up to 72 hrs
  • Can occur w/ or w/o aura
    • Migraine w/ aura- sometimes preceded/ accompanied by focal neurological symptoms eg visual symptoms such as zigzag lines, scrotoma (area of partial alteration in visual field), sensory symptoms such as pins and needles
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62
Q

Which gender is more likely to be affected by migraine?

A
  • Female
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63
Q

What are the diagnostic characteristics of a migraine?

A

ICHD criteria-

  1. At least 5 attacks fulfilling criteria B-D
  2. Headache attacks lasting 4-72 hrs (when untreated or unsuccessfully treated)
  3. Headache has at least 2 of the following characteristics-
    • Unilateral location
    • Pulsating quality
    • Moderate or severe pain intensity
    • Aggravation by or causing avoidance of routine physical activity eg walking or climbing stairs
  4. During headache at least 1 of the following-
    • N/V
    • Photophobia or phonophobia
  • Not better accounted for by another ICHD-3 diagnosis
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64
Q

Suggest some common triggers for a migraine attack?

A
  • Tired, stress
  • Alcohol
  • COCP
  • Lack of food/ dehydration
  • Cheese, chocolate, red wines, citrus fruits
  • Menstruation
  • Bright lights
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65
Q

Describe the acute treatment of a migraine?

A
  • First line: combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol
  • For young people age 12-17 consider nasal triptan over an oral triptan
  • If the above measures are not effective or tolerated offer non-oral metoclopramide or prochlorperazine and consider adding a n on-oral NSAID or triptan
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66
Q

Who gets prophylaxis for migraine? Describe the treatment options available for prophylaxis of a migraine?

A
  • Prophylaxis given if patients are experiencing 2 or more attacks per month
  • NICE advise either topiramate or propranolol
    • Propanolol should be preferred in women of child-bearing age
  • 10 sessions of acupuncture over 5-8 weeks
  • Riboflavin (400mg once daily) may be effective in reducing migraine frequency & intensity for some people
  • Predictable menstrual migraine
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67
Q

How to approach treatment of migraine?

A
  • Non-tablet options
    • Hydration
    • Rest
    • Avoid triggers- diary of foods for ~8wks
    • Wt loss
    • Exercise
    • Cold and hot compress
    • Massage to forehead & temples
    • ‘4-head’
  • Acute mx
    • Simple analgesia- NSAID, paracetamol
    • Triptan (5HTl-receptor agonist)- sumatriptan, take at onset of headache, can be repeated after a couple of hours 2 times a day
      • Contraindicated in cardiovascular disease, peripheral vascular disease, pregnancy
      • Causes vasoconstriction
    • Antiemetic
  • Prophylaxis
    • Start at low dose, gradually increase according to response to maximum tolerated dose
    • Amitriptyline, propranolol, atenolol, verapamil, gabapentin, topiramate
  • If they don’t respond to at least 3 prophylactic meds + exclude medication overuse
    • Botox- 3 monthly injections, headache diary
    • Calcitonin gene-related peptide (CGRP) receptor antagonists
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68
Q

What is analgesic overuse headache?

A
  • Headache on 15+ days of the month in a pt with pre-existing primary headache & developing as a consequence of regular overuse of acute or symptomatic headache medication for >3mnths
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69
Q

What level of analgesic use constitutes overuse of analgesics?

A
  • Simple analgesics eg NSAIDs, paracetamol- for 15 days or more per month
  • Ergotamine, triptans, opioids, combination analgesics- for 10 days or more per month
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70
Q

What is the management of medication overuse headache?

A
  • Withdrawal of the overused drug
    • Stop simple analgesics abruptly for 6 wks minimum
    • Withdraw codeine over 2-4 wks- can use naproxen for 2 weeks intermittently to help the pain
  • Advice for pt-
    • Pt may feel worse initially
    • Keep a headache diary
    • After 6 weeks, simple analgesics can be used on no more than 10 days a month
    • Codeine should be avoided in chronic headache
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71
Q

Describe the clinical features and management for a tension headache

A
  • Clinical features: tight band around the head or pressure sensation, bilateral symptoms, lower intensity than migraine, no aura/ N&V/ aggravated by routine physical activity
  • Mx- aspirin, paracetamol or NSAID first line for acute treatment
    • Prophylaxis- up to 10 sessions of acupuncture over 5-8 weeks
    • Low dose amitriptyline is widely used but not recommended by NICE
  • If there is no improvement or diagnostic uncertainty, refer to neurology
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72
Q

Who commonly suffers from tension headaches?

A
  • Patients in their 20s
  • Stress, mental tension
  • Fatigue
  • Missing meals
  • Female > male
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73
Q

What is a cluster headache?

A
  • A severe primary headache disorder characterised by recurrent unilateral headaches centred on the eye or temporal region
  • Occur in short attacks (15-180mins)
  • Associated w/ ipsilateral autonomic signs
    • Conjunctival injection (enlargement of conjunctival vessels)
    • Nasal congestion
  • May be episodic with periods of remission or chronic (no periods of remission for >3 months)
  • Most common trigeminal autonomic cephalgia (TAC)
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74
Q

What are trigeminal autonomic cephalalgias?

A
  • TACs are a group of primary headache disorders characterised by:
    • Unilateral pain within the trigeminal distribution
    • Associated ipsilateral cranial autonomic features
      • Such as lacrimation, conjunctival injection, rinorrhoea, nasal congestion, eyelid oedema, ptosis
  • Most common type of TAC: cluster headache
  • Other types- paroxysmal hemicrania (PH), SUNCT (short-lasting uniltaral neuralgiform headache attacks with conjunctival injection and tearing), hemicrania continua
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75
Q

What is the diagnostic criteria for a cluster headache?

A
  1. At least 5 attacks fulfilling criteria 2-4
  2. Severe or very severe unilateral orbital, supraorbital +/- temporal pain lasting 15-180 mins (when untreated)
  3. At least one of the following symptoms/ signs ipsilateral to the headache
    • Conjunctival injection or lacrimation
    • Nasal congestion or rinorrhoea
    • Eyelid oedema
    • Forehead and facial sweating
    • Miosis +/- ptosis
    • Sense of restlessness or agitation
  4. Occurring with a frequency between 1 to 8 a day
  5. Not better accounted by another ICHD-3 diagnosis
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76
Q

List a few differentials for cluster headache?

A
  • Age >50: GCA, SoL
  • Age <10: secondary causes?
  • Immunodeficient: malignancy, infection
  • Active/ previous cancer: metastatic spread
  • Pregnant: pre-eclampsia, venous sinus thrombosis
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77
Q

Risk factors for suffering from cluster headaches?

A
  • Male
  • Smokers
  • Alcohol
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78
Q

How are cluster headaches treated?

A
  • First-line: sumatriptan for acute attacks
    • 5HT1-receptor agonist
    • Route: subcutaneous or intranasal
  • Short burst O2 therapy- 15 L/min via non-rebreather mask for 15-20 mins
  • Avoid triggers
  • Prevention medication: verapamil
    • Calcium channel blocker
  • Refractory disease- where medical options haven’t helped, there are a few therapies available-
    • Greater occipital nerve blocks
    • Deep brain stimulation
    • Trigeminal nerve compression
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79
Q

Movement disorders arise from pathology where?

A
  • Basal ganglia
  • Insufficiency of neurotransmitter dopamine
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80
Q

What is the normal function of the basal ganglia?

A
  • The basal ganglia is a series of cell bodies (grey matter) that are located together within the deep subcortical white matter of the brain
  • Stimulate motor cortex
  • Responsible for coordinating habitual movements such as walking or looking around, controlling voluntary movements and learning specific movement patterns
  • Part of the basal ganglia called the substantia nigra produces a neurotransmitter: dopamine, which is essential for the correct functioning of the BG
  • In PD, there is gradual but progressive fall in dopamine production
  • The thalamus is not formally classified as part of the basal ganglia, forms extensive connections with nuclei
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81
Q

What are some of the important functions of the basal ganglia?

A
  • Inhibition of muscle tone
  • Co-ordinated, slow, sustained movement
  • Suppression of useless patterns of movement
  • Initiation of movement
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82
Q

How are movement disorders classified?

A
  • Hypokinetic- Parkinson’s disease, Parkinson’s plus syndromes- PSP, MSA, CBD, AD with Lewy bodies
  • Hyperkinetic- tremor, dystonia, myoclonus, chorea, tics, akathisia
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83
Q

What is idiopathic Parkinson’s Disease?

A
  • IPD is a progressive degenerative disorder characterised by neuronal loss in the brain stem and basal ganglia
  • There is loss of dopaminergic neurones in the substantia nigra that leads to inadequate dopamine transmission
    • PD may not be apparent until a substantial number of neurones (50-80%) have been lost within the substantia nigra
  • Lewy Body formation in affected neurones is a characteristic finding
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84
Q

What are the 3 classic clinical features of Parkinson’s disease?

A
  1. Bradykinesia
    1. General slowing of voluntary movements
    2. ↓ arm swing
    3. ↓ in amplitude with repetitive movements
  2. Tremor (unilateral)
    1. Resting & pill-rolling
    2. 4-6Hz in frequency
    3. Can be induced by distraction
  3. Rigidity
    1. ↑ resistance to passive movement in a joint
    2. Cogwheel due to superimposed tremor
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85
Q

What are the symptoms of Parkinson’s disease?

A
  • Motor symptoms
    • Akinetic rigid amalgamation of symptoms:
      • Unilateral rolling tremor
      • Rigidity
      • Bradykinesia- slowness of voluntary movements
      • Unsteady gait- slowness of movements, reduced arm swing (can be asymmetrical at the beginning of PD), forward flexion (later), small shuffling steps, defragmentation of turns, reduced postural control and stability, hesitancy in initiating movement
      • Postural instability- most disabling features
  • Non motor symptoms
    • Fatigue
    • Orthostatic hypotension
    • Bladder & bowel dysfunction
    • REM sleep disorders
    • Saliva drool
    • Depression
    • Dementia
    • Hallucinations, delusions
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86
Q

What is the typical patient with Parkinson’s Disease?

A
  • Older aged man around 70 years old
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87
Q

Describe the tremor in Parkinson’s Disease?

A
  • Unilateral
  • Pill rolling: looks like they are rolling a pill between their fingertips & thumb
  • More pronounced when resting
  • Improves on voluntary movement
  • Worsened if pt is distracted
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88
Q

What is meant by cogwheel rigidity?

A
  • If you take their hand & passively flex & extend their arm at the elbow, you feel a tension in their arm that gives way to movement in small increments (like little jerks) à cogwheel
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89
Q

How can bradykinesia present in a patient with PD?

A
  • Handwriting gets smaller and smaller
  • Can only take small steps when walking- shuffling gait
  • Difficulty initiating movement- eg when standing still to walking
  • Difficulty in turning around when standing- have to take lots of small steps
  • Reduced facial movements and facial expression- hypomimia
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90
Q

Describe what happens to the gait in Parkinson’s disease?

A
  • Slow movement
  • Reduced arm swing
  • Forward flexion
  • Shuffling gait
  • Defragmentation of turns
  • Reduced postural control & stability
  • Hesitancy in initiating movement
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91
Q

How is Parkinson’s Disease diagnosed?

A
  • Bradykinesia
  • At least one of the following-
    • Muscular rigidity
    • 4-6 Hz rest tremor
    • Postural instability not caused by primary visual, vestibular, cerebellar or proprioceptive dysfunction
  • 3 or more required for diagnosis of definite PD in combination with the above
    • Unilateral onset
    • Rest tremor present
    • Progressive disorder
    • Persistent asymmetry affecting side of onset most
    • Excellent response (70-100%) to levodopa
    • Severe levodopa-induce chorea
    • Levodopa response for 5 years or more
    • Clinical course of 10 years or more
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92
Q

List some Parkinson’s-plus syndromes?

A
  • Multiple system atrophy- where the neurones of multiple systems in the brain degenerate, affects BG & other areas, leads to Parkinson’s presentation
    • Degeneration of other areas à autonomic dysfunction: postural hypotension, constipation, abnormal sweating, sexual dysfunction
    • Cerebellar dysfunction à ataxia
  • Dementia with Lewy Bodies: associated features of Parkinsonism, progressive cognitive decline, visual hallucinations, delusions, disorders of REM sleep & fluctuating consciousness
  • Progressive supranuclear palsy
  • Corticobasal degeneration
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93
Q

How is Parkinson’s Disease treated?

A
  • Levodopa
    • Reduces the motor symptoms (not effective on non-motor)
    • Carbidopa prevents peripheral breakdown of levodopa
    • à combination drugs: co-benyldopa, co-careldopa
    • Doesn’t alter disease progression
    • More motor complications
  • COMT inhibitors- entacapone, tolcapone
  • Dopamine agonists- ropinirole
    • Doesn’t reduce motor symptoms as much as levodopa
  • Amantadine
  • MAO inhibitors
  • Surgical
    • Deep brain stimulation
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94
Q

What are the commonly used medications for treating IPD along with their mode of action and major side effects?

A
  • Dopaminergic drugs- levodopa (as co-careldopa, co-beneldopa)
    • L-dopa is a precursor of dopamine that can enter the brain via a membrane transporter
    • In PD there is a deficiency of dopamine in the nigrostriatal pathway that links the substantia nigra in the midbrain to the corpus striatum in the basal ganglia – this causes the basal ganglia to exert greater inhibitory effects on the thalamus, ↓ the excitatory input to the motor cortex, hence the features of PD such as bradykinesia and rigidity – replacing the dopamine will counteract this
    • Levodopa: wearing off effect where the pt’s symptoms worsen towards the end of the dosage interval- can be overcome by increasing the dose/ frequency, but this can cause dyskinesia and excessive movements at the beginning of the dosage interval = the on-off effect
    • When the dose of dopamine is too high, pts can develop dyskinesia- excessive motor activity
      • Dystonia: excessive muscle contraction leads to abnormal postures or exaggerated movements
      • Chorea: abnormal involuntary movements that can be jerking or random
      • Athetosis: involuntary twisting or writhing movements usually affecting fingers, hands or feet
  • COMT inhibitors (entacapone)
    • Inhibition of catechol-o-methyltransferase which metabolises levodopa in both the body and brain
    • Entecapone is taken with levodopa to slow breakdown of the levodopa in the brain, extends the effective duration of levodopa
  • Dopamine agonists (ropinirole, pramipexol)
    • Ropinirole and pramipexol are relatively selective agonists for D2 receptor
    • Usually used to delay the use of levodopa and are then used in combination with levodopa to reduce the dose required
    • One notable side effect is pulmonary fibrosis
  • All dopaminergic drugs can cause nausea, drowsiness, confusion, hallucinations, hypotension
  • Monoamine oxidase inhibitors (selegiline, rasagiline)
    • Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin & adrenaline; most specific to dopamine, helps increase circulating dopamine
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95
Q

Why is levodopa given with a peripheral dopa-decarboxylase inhibitor?

A

Why is levodopa given with a peripheral dopa-decarboxylase inhibitor?

  • To reduce its conversion to dopamine outside the brain
  • This ↓ nausea and lowers the dose needed for therapeutic effect
96
Q

What is the first-line treatment for Parkinson’s Disease?

A
  • First line is levodopa if motor symptoms are affecting pt’s QoL
  • If motor symptoms are not affecting QoL, dopamine agonist, levodopa or MAO B inhibitor can be used
97
Q

Non-oral treatments are sometimes used for IPD, when and why? List some of the non-oral treatments used in these circumstances?

A
  • Nearly all pts with IPD respond well to drug treatment but as the disease advances response becomes poorer and side effects from the drugs can be disabling, in these instances non-oral treatments are sometimes used
98
Q

List a few members of the MDT involved in caring for PD patients?

A
  • Medical specialist- neurologist or geriatrician
  • PD specialist nurse
  • Physiotherapist
  • Occupational therapist
  • Speech and language specialist
  • Dietician later states
  • Psychiatrist sometimes required
99
Q

What are the 4 recognised distinct phases of Parkinson’s disease?

A
  1. Early stage- soon after diagnosis, mild symptoms, normal life possible
  2. Maintenance- good response to treatment, no major disability
  3. Advanced stage- poor response to drugs with motor side effects
  4. Palliative stage- unable to live independently and in need of MD support
100
Q

Describe the complications that are seen in advancing IPD

A
  • Motor complications: deteriorating function, loss of drug effect, motor fluctuations, dyskinesia, freezing of gait, falls
  • Non-motor:
    • Mental health: depression, anxiety, apathy
    • Dementia, cognitive impairment
  • Autonomic dysfunction: constipation, orthostatic hypotension, dysphagia, weight loss, XS sweating & salivation, bladder & sexual problems
  • Other: N&V, pain, sleep disturbance, aspiration pneumonia, pressure sores
101
Q

What is Parkinsonism?

A
  • A syndrome which manifests as bradykinesia and rigidity +/- tremor +/- postural instability
102
Q

What are some causes of Parkinsonism?

A
  • Multiple System Atrophy (MSA)
  • Progressive Supranuclear Palsy (PSP)
  • Dementia with Lewy bodies
  • Drug-induced Parkinsonism- antipsychotics, metoclopramide, antidepressants
  • Wilson’s disease
  • Post-encephalitis
  • Toxins: carbon monoxide, MPTP
103
Q

Why does domperidone not cause extra-pyramidal effects?

A
  • Doesn’t cross Blood Brain Barrier
104
Q

How does an essential tremor present?

A
  • Typically an essential tremor is a postural tremor (worse if arms outstretched) but may also be intentional
    • Postural- ask pt to hold their hand it happens, intention- trying to move hand and can’t
  • Typically bilateral- generally affects the dominant side more than the non-dominant side
  • Fine tremor, symmetrical, more common on voluntary movements
  • Worse when tired, stressed or after caffeine
  • Improved by alcohol
  • Absent during sleep
  • Most common cause of titubation (head tremor)
  • FHx
  • No features of PD present- none of the postural stability, masked faces, cog wheeling, non-motor symptoms
  • Check thyroid- hyperthyroidism can lead to tremor
105
Q

What are some risk factors/ causes of essential tremor?

A
  • Ageing
  • Genetics
  • Environmental toxins- pesticides, lead, mercury
106
Q

What are some exacerbating/ relieving factors for an essential tremor?

A
  • Alcohol & rest both improve tremor
  • Exacerbated by anxiety, excitement, adrenergic stimulation
107
Q

How to differentiate essential tremor from Parkinson’s disease?

A
  • Archimedes spiral test for tremor diagnosis
  • Essential tremor: 8 to 2 O’clock
108
Q

What are some differentials of a tremor?

A
  • Parkinson’s disease
  • Multiple sclerosis
  • Huntington’s chorea
  • Hyperthyroidism
  • Fever
  • Medications- antipsychotics
109
Q

How is an essential tremor managed?

A
  • 1st line: propranolol
  • Primidone is also sometimes used
  • Both the above medications may reduce the tremor amplitude by up to 50% however the tremor may not completely subside
110
Q

Describe the anatomy of the brainstem

A
  • Midbrain (mesencephalon)
    • Cerebral peduncles- connect cerebral hemisphere to midbrain, descending motor fibres down into cord
  • Pons
  • Medulla
    • Medullary pyramids- decussation of descending motor fibres- lateral corticospinal tracts
111
Q

Where are upper motor neurones found?

A
  • Primary motor cortex (precentral gyrus)
  • Upper limb- lateral aspect of motor cortex
  • Lower limb- medial aspect of motor cortex
112
Q

What is the net effect of UMNs on LMNs?

A
  • Inhibition
113
Q

Why do UMN lesions involving the face spare the forehead?

A
  • The facial motor nucleus is split into 2 halves, 1 supplies superior face and one inferior face
  • The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres, whereas the part that supplies the lower face only receives a contralateral UMN input
  • Hence UMN lesions involving the face spare the forehead
  • True face nerve palsies- affects all muscles of facial expression
114
Q

Signs of UMN damage? What happens in the acute phase of an UMN lesion?

A
  • Damage to upper motor neurones means loss of descending inhibition of lower motor neurones
  • Weakness (loss of direct excitatory inputs onto LMNs from UMNs)
  • Hypertonia (loss of descending inhibition)- all muscles affected equally however in the U/L the flexors are more powerful so they win
    • Flexed upper limb
    • Extended lower limb
  • Hyperreflexia (brisk reflexes due to
  • Extensor plantar reflexes
  • Positive Babinski sign (loss of descending modulation of spinal reflexes)
  • Clonus (exaggerated stretch reflexed causes a series of contractions in a muscle when it is suddenly stretched & held in that position)
  • Clasped knife rigidity- gives way
  • Long term disuse of a muscle due to paralysis à disuse atrophy
  • Acute phase of UMN lesion:
    • Flaccid paralysis- spinal shock – converts to hypertonia after a few weeks
115
Q

Describe some signs for UMN vs LMN?

A
  • UMN: hypertonia, hyperreflexia, spasticity, positive Babinski’s sign, clonus
  • LMN: hypotonia, hyporeflexia, flaccid weakness, fasciculations, atrophy
116
Q

Where are LMN cell bodies found?

A
  • The cell body of a LMN lies with the central nervous system
    • Ventral horn of spinal cord
    • Brainstem motor nuclei of the cranial nerves which have motor modalities- oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus
117
Q

When LMN are damaged, what signs can be seen in the muscles they supply?

A
  • Weakness (due to denervation)
  • Hyporeflexia/ areflexia (due to denervation)
  • Wasting (due to loss of trophic support to the muscle from the LMN across the NMJ)
  • Hypotonia (due to loss of muscle activation)
  • Fasciculation (involuntary muscle twitches, often compared to having a bag of worms under the skin, due to loss of up-regulation of muscle nAChRs to try to compensate denervation)
118
Q

Causes of UMN damage?

A
  • Stroke, MS, traumatic brain injury, cerebral palsy, spinal cord injury, Huntington’s disease
119
Q

Causes of LMN damage?

A
  • Motor neurone disease
  • Peripheral neuropathy
  • Poliomyelitis
  • Spinal cord injury with nerve root compression
  • Spinal muscular atrophy
120
Q

What is spinal muscular atrophy?

A
  • Autosomal recessive
  • Loss of motor neurones within ventral horn of spinal cord and motor nuclei of cranial nerves in pons/ medulla
  • Signs of LMN syndrome
  • Often accompanying bulbar palsy
121
Q

Causes of peripheral neuropathy?

A
  • Can be divided into conditions which predominantly cause a motor or sensory loss
  • Predominantly motor loss
    • Guillain-Barre syndrome
    • Porphyria
    • Lead poisoning
    • Charcot-Marie-Tooth
    • Chronic inflammatory demyelinating polyneuropathy (CIDP)
    • Diphtheria
  • Predominantly sensory loss
    • Diabetes
    • Uraemia
    • Leprosy
    • Alcoholism
    • B12 deficiency
    • Amyloidosis
  • ABCDE mnemonic:
    • Alcohol
    • B12 deficiency
    • Cancer and CKD
    • Diabetes and Drugs (isoniazid, amiodarone, cisplatin)
    • Every Vasculitis
122
Q

What is Guillain-Barre syndrome?

A
  • Immune-mediated demyelination of the peripheral nervous system, acute paralytic polyneuropathy
  • Triggers- often infection- Campylobacter jejuni
  • Molecular mimicry
    • Antibodies against the antigen on the pathogen that causes the pre-ceding infection
    • The antibodies also match the proteins on the nerve cells
    • They may target proteins on the myelin sheath or the nerve axon
  • Cross-reaction of antibodies with gangliosides in the PNS
  • Correlation between anti-ganglioside antibody (eg anti-GM1) and clinical features has been demonstrated
123
Q

How does Guillain-Barre syndrome present?

A
  • Initially- back or leg pain
  • Characteristic features- progressive, symmetrical weakness of all limbs – starts at feet and moving up body
    • The weakness is classically ascending i.e. legs affected first
    • Reduced or absent reflexes
    • Sensory symptoms tend to be mild- eg distal paraesthesia
    • Neuropathic pain may be present
  • May be a hx of a gastroenteritis
  • Respiratory muscle weakness
  • Cranial nerve involvement-
    • Diplopia4
    • Bilateral facial nerve palsy
    • Oropharyngeal weakness
  • Autonomic involvement-
    • Urinary retention
    • Diarrhoea
  • Less common- papilledema secondary tor educed CSF resorption
124
Q

Describe the course of symptoms in GBS?

A
  • Symptoms start within 4 weeks of preceding infection
  • Symptoms typically start in feed and progresses upward
  • Peaks 2-4 weeks
  • Recovery period months- years
125
Q

How is a diagnosis of GBS made?

A
  • Clinical diagnosis- Brighton criteria to diagnose & distinguish high/ low risk
  • Nerve conduction studies- reduced signal through the nerves
  • Lumbar puncture for CSF- raised protein w/ normal cell count + glucose
126
Q

Describe the management of GBS?

A
  • IV immunoglobulins
  • Plasma exchange- removes the circulating antibodies
  • Supportive care
    • Respiratory failure- monitor FVC
    • Cardiovascular monitoring
    • VTE prophylaxis (PE is a leading cause of death)
    • Analgesia
127
Q

What is the most common form of Guillain Barre syndrome?

A
  • AIDP: acute inflammatory demyelinating polyneuropathy
  • Classical symptoms of GBS: progressive symmetrical weakness in limbs, reduced or absent tendon reflexes, reduced sensation
  • Over a period of weeks to months remyelination will heal the lesions
128
Q

Acute bulbar palsy

A
  • Rare variant of GBS
129
Q

What is CIDP?

A
  • Chronic inflammatory demyelinating polyneuropathy
  • Symmetrical
  • Slowly progressive & cyclical
130
Q

What is Charcot Marie Tooth disease?

A
  • Hereditary peripheral neuropathy – affects peripheral motor and sensory nerves
  • Causes dysfunction in the myelin or in the axons
  • Hx of frequently sprained ankles
  • Foot drop
  • High arched feet pes cavus
  • Hyporeflexia
  • (relatively common- 1 in 2500 people- likely to appear in OSCE due to good neuro signs)
131
Q

What are the classical features of CMT disease?

A
  • High foot arches (pes cavus)
  • Distal muscle wasting causing inverted champagne bottle legs
  • Weakness in lower legs- loss of ankle dorsiflexion
  • Weakness in hands
  • Reduced tendon reflexes
  • Reduced muscle tone
  • Peripheral sensory loss
132
Q

How is Charcot Marie Tooth disease managed?

A
  • Supportive
  • Orthopaedics: correct disabling joint deformities, physiotherapists: maintain muscle strength and joint range of motion, podiatrists: help with foot problems & prescribe insoles and other orthoses to improve symptoms
133
Q

What is motor neurone disease? What is the commonest type and classical presentation?

A
  • Progressive degeneration of both upper and lower motor neurones- due to degeneration in both UMN and LMN (anterior horn cells) in the spinal cord and brainstem; rapid progression & poor prognosis
  • Sensory neurones are spared
  • Types-
    • Amyotrophic lateral sclerosis- most common, LMN signs in arms and UMn signs in legs
    • Progressive bulbar palsy- second most common, loss of brainstem motor nuclei, affects primarily muscles of talking + swallowing, worst prognosis
    • Progressive muscular atrophy- LMN signs only, affects distal muscles first, best prognosis
    • Primary lateral sclerosis- UMN signs only
  • Typical presentation-
    • Late middle-aged man (eg age 60)
    • Insidious, progressive weakness of muscles throughout the body affecting limbs, trunk, face, speech
    • Weakness often first noticed in upper limbs
    • Increased fatigue when exercising
    • Clumsiness, dropping things more often, dysarthria (slurred speech)
    • No cerebellar signs
  • Signs of LMN- muscle wasting, reduced tone, fasciculations, reduced reflex
  • Signs of UMN- increased tone or spasticity, brisk reflexes, upgoing plantar responses
134
Q

What are some differentials for motor neurone disease?

A
  • Cervical radiculopathy
  • Syringomyelia
  • Syphilic pachymeningitis
  • Motor neuropathy
  • Spinal muscular atrophies
  • Kennedy’s syndrome “spinal and bulbar muscular atrophy)
135
Q

Describe the clinical features and prognosis of the following variants: amyotrophic lateral sclerosis and progressive bulbar palsy

A
  • Amyotrophic lateral sclerosis: typically LMN in arms and UMN in legs, prognosis 3-5 years
  • Progressive bulbar palsy: palsy of tongue, chewing/ swallowing muscles and facial muscles due to loss of brainstem motor nuclei
    • Carries worse prognosis, 1-3 years
136
Q

How is motor neurone disease diagnosed and managed?

A
  • Diagnosis
    • Clinical diagnosis- hx and examination
    • Nerve conduction studies will show normal motor conduction; excludes neuropathy, shows evidence of wide spread denervation
      • NCS is the most useful test
    • Electromyography (EMG)- confirms diagnosis- reduced a.p.’s with increased amplitude
    • MRI cervical spine & brain- exclude cervical cord compression, myelopathy, spinal spondylitis
  • Incurable
  • MDT-
    • Respiratory support- NIV to support breathing at night- BIPAP
    • Nutritional support
    • Psychological support
  • Riluzole
    • Glutamate inhibitor
    • Can slow progression in ALS
    • Prolongs life by ~3 months
  • End of life care planning
137
Q

What do patients with motor neurone disease usually die from?

A
  • Respiratory failure
    • Breathlessness on exertion or when lying flat
    • O/E: poor inspiratory effort, lack of abdo movement w/ respiration
    • Ix: ABG, CO2 retention
    • CXR: hemi-diaphragm
    • Treatment: ventilation support (NIV)
  • Aspiration pneumonia
    • Difficulty swallowing secretions
    • Chronic (silent aspiration)
138
Q

What is myasthenia gravis?

A
  • Autoimmune condition that causes muscle weakness that gets progressively worse w/ activity & improves w/ rest
139
Q

Describe the pathophysiology of myasthenia gravis?

A
  • Acetylcholine receptor antibodies are produced
  • These bind to the post-synaptic nmj receptors
  • This blocks the receptor and prevents the Ach from being able to stimulate the receptor & trigg er muscle contraction
  • As the receptors are used more during activity, more of them become blocked up
  • This leads to less effective stimulation of the muscle with increased activity
  • There is more muscle weakness the more the muscles are used
  • This improves w/ rest as the receptors are freed up again
  • These antibodies also activate the complement system within the nmj leading to damage to cells at the postsynaptic membrane, this further worsens the symptoms
  • There are 2 other antibodies which cause 15% of MG cases
    • Muscle-specific kinase (MuSK)
    • Antibodies against low-density lipoprotein receptor-related protein 4 (LRP4)
140
Q

How do pts with MG present?

A
  • Most symptoms affect the proximal muscles and small muscles of the head and neck
  • Diplopia due to extraocular muscle weakness
  • Ptosis due to eyelid weakness
  • Facial movements weakness
  • Dysphagia
  • Fatigue in jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
  • Strong link with thymoma
141
Q

How can you elicit fatiguability in the muscles in a patient with MG?

A
  • Repeated blinking- ptosis
  • Prolonged upward gazing- diplopia
  • Repeated abduction of 1 arm 20 times- unilateral weakness when comparing both sides
142
Q

How is a diagnosis of myasthenia gravis made?

A
  • Ach-R antibodies (85% pts)
  • MuSK antibodies (10% pts)
  • LRP4 antibodies (<5% pts)
  • CT or MRI of thymus for thymoma
  • Edrophonium test if there is doubt about the diagnosis
    • Given IV edrophonium chloride or neostigmine
    • Stops breakdown of Ach
    • Relieves the weakness temporarily & briefly
143
Q

Describe the mx of myasthenia gravis?

A
  • Long-acting Ache inhibitors: pyridostigmine is first line
  • Immunosuppression: initially prednisolone, azathioprine
  • Thymectomy
  • Monoclonal antibodies
144
Q

What is myasthenic crisis and how is it managed?

A
  • Acute worsening of symptoms
  • Often triggered by RTI
  • Mx- NIV with BiPAP or full intubation and ventilation
  • Immunomodulatory therapies- IV immunoglobulins and plasma exchange
145
Q

List some drugs that may exacerbate myasthenia?

A
  • Penicillamine
  • Quinidine, procainamide
  • Beta blockers
  • Lithium
  • Phenytoin
  • Abx: gentamicin, macrolides, quinolones, tetracyclines
146
Q

What is multiple sclerosis, what part of the nervous system does it affect?

A
  • Central nervous system- oligodendrocytes
  • Inflammation around myelin and infiltration of immune cells causing demyelination
  • Characterised by plaques
147
Q

What are some risk factors for multiple sclerosis?

A
  • Viral infections- EBV
  • Geographic latitude- prevalence of MS increases the greater the distance north or south from the equator
  • Sunlight exposure- inverse relationship- low vitamin D
  • Other- obesity during adolescence, smoking, gender (females)
148
Q

What are some classical plaque sites in multiple sclerosis?

A
  • Optic nerves
  • Spinal cord- cervical spine
  • Brainstem- ophthalmoplegia
  • Cerebellum- ataxia & gait disturbance
  • Juxtacortical white matter- near the cerebral cortex
  • Periventricular white matter
  • A characteristic feature of MS is that lesions vary in their location over time
149
Q

What are some clinical presentations of MS?

A
  • Optic neuritis (mx = high dose steroids, recovery within 4-6 weeks)
  • Diplopia
  • Ascending sensory disturbance +/- weakness particularly in face or limbs
  • Weakness due to UMN
  • Problems with balance, unsteadiness, clumsiness
  • Altered sensation travelling down the back and sometimes into the limbs when bending the neck forwards (lhermitte’s symptom)
  • Neuropathic pain eg trigeminal neuralgia
  • Bladder symptoms
  • Cognitive impairment (usually a late sign)
  • Pts are often <50 years old, have a hx of previous neurological symptoms, have symptoms that have evolved over >24 hours, have symptoms that may persist over several days/ weeks and then improve
150
Q

What are the key visual clinical features of multiple sclerosis?

A
  • Visual loss
  • Blurred vision
  • Pain typically behind the eye and on movement
  • Scotoma- partial visual field loss
  • Poor colour differentiation
  • Relative afferent pupillary defect
  • Optic nerve swelling
  • INO: intranuclear ophthalmoplegia
  • Abducens palsy
151
Q

List some causes of optic neuritis?

A
  • Multiple sclerosis: the commonest associated disease
  • Sarcoidosis
  • SLE
  • Diabetes
  • Syphilis
  • Measles
  • Mumps
  • Lyme disease
152
Q

What are the features of optic neuritis?

A
  • Unilateral decrease in visual acuity over hours or days
  • Poor discrimination of colours, red desaturation
  • Pain worse on eye movement
  • RAPD
  • Central scrotoma
153
Q

What are the features of trigeminal neuralgia?

A
  • Severe unilateral pain
  • Brief electric shock-like pains, abrupt in onset & termination, limited to 1 or more divisions of trigeminal nerve
  • Pain commonly evoked by light touch, washing, shaving, smoking, talking, brushing teeth or can be spontaneous
  • Small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
  • The pins usually remit for variable periods
154
Q

How does intranuclear ophthalmoplegia occur in multiple sclerosis?

A
  • Disorder of conjugate lateral gaze due to demyelination of the medial longitudinal fasciculus (MLF)
  • MLF is heavily myelinated
  • Connects the abducens nucleus complex with the contralateral oculomotor nucleus
  • If affected, when looking to the R, the R eye will abduct but the L will remain central (failure in adduction)
155
Q

What sort of motor abnormalities occur in MS?

A
  • Progressive paraparesis
  • Evidence of UMN signs- spasticity, reduced power, hyper-reflexia
  • Transverse myelitis
  • Cerebellar syndrome
156
Q

What are some sensory and autonomic symptoms that can occur in multiple sclerosis?

A
  • Paraesthesia
  • Pain
  • Heat sensitivity (Uhthoff phenomenon)
  • Sexual dysfunction
  • Bladder & bowel dysfunction
157
Q

Suggest some psychological symptoms that can occur in MS?

A
  • Cognitive impairment
  • Depression
  • Fatigue
  • The depression can have a negative impact on memory, attention & concentration
158
Q

There are 3 main patterns of multiple sclerosis- what are they and describe the differences in these 3 variants?

A
  • Relapsing-remitting MS (RMMS)
    • Most common at initial diagnosis
    • Active: new symptoms are developing or new lesions are appearing on MRI or not active where no new symptoms or lesions are appearing on MRI
    • Overall worsening disability over time or no worsening
  • Secondary progressive MS (SPMS)
    • Where there is relapsing-remitting MS but with progressive worsening of symptoms with incomplete remissions, symptoms become more and more permanent
  • Primary progressive MS (PPMS)
    • Where there is worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions, classified as active or worsening
159
Q

How is a diagnosis of multiple sclerosis made?

A
  • MS attack- an episode of neurological symptoms that relate to an inflammatory demyelinating lesion, lasts >24 hours +/- recovery, typically sensory/ motor/ visual disturbances, 30+ days between episodes
160
Q

What is the Mcdonald criteria for multiple sclerosis?

A
  • Lesions consistent with an inflammatory process
  • No alternative diagnosis
  • Multiple lesions in time and space (relapsing-remitting MS)
  • Progressive neurological deterioration for 1 year (primary progressive MS)
161
Q

When might a relapse be diagnosed in an MS patient?

A
  • Develops new symptoms
  • Has rapid worsening of existing symptoms
  • Symptoms last for more than 24 hours in the absence of infection or other cause after a stable period of 1 month or more
162
Q

What are some differential diagnoses of MS?

A
  • Demyelinating diseases- transverse myelitis, acute disseminated encephalomyelitis
  • Infections- lyme disease
  • Metabolic disease- B12 deficiency, diabetic neuropathy, adult onset leukodystrophies, copper deficiency
  • Systemic diseases: SLE, sarcoidosis
  • Other: neoplasia, vasculitis, stroke
163
Q

What are some useful investigations for MS?

A
  • MRI of brain or spinal cord- demonstrates demyelination plaques
  • Immunoelectorphoresis of CSF- shows oligoclonal bands of IgG
164
Q

Describe the role of a lumbar puncture in patients with MS?

A
  • Analyse CSF to assess for CSF-specific oligoclonal bands
  • Oligoclonal bands = bands of immunoglobulins
  • The test is positive if oligoclonal bands identified in the CSF are not present in the serum
165
Q

Describe the management of multiple sclerosis?

A
  • General care- modifiable risk factors
    • Exercise to maintain strength
    • Vaccinations- live vaccines may be contraindicated
    • Possible benefit of flu vaccine
    • Advise not to smoke
    • Advise that MS-related fatigue may be precipitated by heat, overexertion, stress, time of day
  • Managing acute relapses
    • Methylprednisolone 500mg po od for 5 days, 1g IV for 3-5 days where oral treatment has failed previously/ severe relapse
  • Disease modifying therapies
  • Symptomatic treatments
    • Neuropathic pain: amitryptiline, gabapentin
    • Depression: SSRIs
    • Urge incontinence: tolterodine, oxybutynin
    • Spasticity: baclofen, gabapentin, physiotherapy
166
Q

What drugs can help the following symptoms in MS: spasticity, neuropathic pain, depression, incontinence, fatigue, paroxysmal symptoms

A
  • Spasticity: baclofen and gabapentin are 1st line, physiotherapy
  • Neuropathic pain: amitriptyline, gabapentin
  • Depression: SSRIs
  • Incontinence: anticholinergics – oxybutynin
  • Fatigue: amantadine
167
Q

List some disease modifying drugs used in MS

A
  • Beta-interferons reduce relapse rate by up to 30%
  • Natalizumab: a recombinant monoclonal antibody that antagonises alpha-4 Beta-1-integrin found on surface of leucocytes, thus inhibiting migration of leucocytes across the endothelium across the BBB
  • Fingolimod: prevents lymphocytes from leaving lymph nodes
168
Q

What is spondylosis?

A
  • The general degeneration of the spine that can occur in joints, discs and bones of the spine as we age
  • Results from osteoarthritis
169
Q

How does cervical spondylosis present?

A
  • Neck pain
  • Referred pain may mimic headaches, shoulder blades/ upper limb pain
  • Orbital/ temporal pain
  • Neck stiffness
  • Poor balance
  • Limited range of movement
  • Radiculopathy due to compression or stretching of the nerve roots- unilateral pain in one dermatome
  • Clinical diagnosis
170
Q

How is cervical spondylosis managed?

A
  • Encourage neck movement and refrain from work absence etc
  • Refer to physiotherapist, psychologist
  • Might need surgery if pain > 12 weeks
171
Q

How does lumbar spondylosis present?

A
  • Pain
  • Stiffness
  • Referred pain to the buttocks or legs
  • Restricted movement
172
Q

How is lumbar spondylosis managed?

A
  • Encourage good posture
  • Keep moving- avoid staying in 1 position
  • Take care when lifting- bend at knees
  • Engage in physiotherapy exercises
  • Lumbar facet injections
  • Corticosteroid injections
  • Surgery- spinal fusion, laminectomy, disc replacement
173
Q

Cause of carpal tunnel syndrome?

A
  • Median nerve compression in the carpal tunnel
  • Idiopathic
  • Pregnancy
  • Oedema- eg HF
  • Lunate fracture
  • Rheumatoid arthritis
174
Q

Clinical features of carpal tunnel syndrome?

A
  • Pins and needles or pain in thumb, index, middle finger
  • Symptoms may ascend proximally
  • Pt shakes hand to obtain relief- classically at night
  • Examination: weakness of thumb abduction (abductor pollicis brevis)
  • Wasting of thenar eminence
  • Tinel’s sign: tapping à paraesthesia
  • Phalen’s sign: wrist flexion causes symptoms
175
Q

Mx of Carpal tunnel syndrome?

A
  • Corticosteroid injection
  • Wrist splints at night
  • Surgical decompression (flexor retinaculum division)
176
Q

What is ulnar nerve palsy caused by?

A
  • Ulnar nerve entrapment at the elbow- cubital tunnel syndrome
  • Ulnar nerve entrapment at wrist- Guyon’s canal syndrome
  • Due to repetitive compression from leading on elbows or wrists and prolonged elbow flexion
  • Can also occur from trauma, swelling, fractures, vascular and bony pathologies
177
Q

How does ulnar nerve palsy present?

A
  • Loss of sensation in hand- ring and little fingers
  • Loss of finger coordination
  • Pain
  • Hand weakness may get worse with physical activity
  • Loss of grip strength
  • Severe cases- ulnar claw
178
Q

How is ulnar nerve palsy managed?

A
  • Splinting
  • NSAIDs
  • Physiotherapy
  • Corticosteroid injection
  • Surgical intervention
179
Q

What is the ulnar paradox?

A
  • High ulnar nerve injury à less prominent ulnar claw
  • Low ulnar nerve injury à more prominent ulnar claw
180
Q

What are the meninges & what is their function? Where is the subarachnoid space?

A
  • The meninges cover the brain and the spinal cord- there are three layers
    • Dura mater (outermost)
    • Arachnoid mater
    • Pia mater (innermost- tightly adhered to surface of brain & spinal cord, followed gyri & fissures)
  • 2 major functions-
    • Supportive framework for cerebral & cranial vasculature
    • Protect CNS from mechanical damage
  • Subarachnoid space
    • Underneath the arachnoid mater
    • Contains cerebrospinal fluid- cushion to brain
    • Arachnoid mater projections (arachnoid granulations_ allow CSF to re-enter the circulation via dural venous sinuses
181
Q

What are some risk factors for subarachnoid haemorrhage?

A
  • Hypertension
  • Smoking
  • Excessive alcohol consumption
  • Cocaine use
  • FHx
  • Black female patients, age 45-70
  • Sickle cell anaemia
  • Connective tissue disorders- Marfan’s, Ehlers-Danlos
  • Neurofibromatosis
182
Q

How likely is it to see evidence of a subarachnoid haemorrhage on plain CT head scan and how much difference does it make if the scan is delayed?

A
  • 90% sensitivity in first 24 hrs
  • 50% sensitivity by 72 hrs
183
Q

If there is a very convincing hx for SAH however the head CT hasn’t shown evidence of a haemorrhage, how would you proceed?

A
  • Lumbar puncture
    • Do not perform within first 12 hrs post headache onset
  • Plain CT head is not 100% sensitive and the consequences of missing a SAH and leaving it untreated are serious
184
Q

Why should you delay a lumbar puncture 12 hrs after a bleed?

A
  • The CSF is analysed by spectrophotometry looking for the bilirubin peak- bilirubin is the breakdown product of blood produced as the blood breaks down over several hours
  • When you perform an LP it is unavoidable there will be some bleeding in the CSF caused by the procedure
  • When the sample is analysed, provided there has been time for the blood from the SAH to start to break down, if there are RBC you can still ascertain that there has been a SAH by the presence of a bilirubin peak
  • If you take the sample too early then there’s no chance for the cells to start to break down & you may not be able to tell whether the RBCs in the CSF are due to a SAH or whether they have been introduced during the LP
185
Q

What are the causes of SAH?

A
  • 70% berry aneurysms
  • 10% arteriovenous malformations
  • 10% hypertension
  • 5% idiopathic
  • Trauma
186
Q

What are the classical presenting features of SAH?

A
  • Headache- sudden-onset, thunderclap, severe, occipital
  • N&V
  • Meningism- photophobia, neck stifness
  • Coma
  • Seizures
  • Sudden death
  • ECG- ST elevation
187
Q

Once a SAH is confirmed via CT or LP, what do you do next?

A
  • Immediate transfer to interventional neuroradiologist or neurosurgical ward for a cerebral angiogram & treatment of any remaining aneurysm or AVM if one is found
    • This will help prevent a re-bleed
  • Give nimodipine (CCB, targets brain vasculature) to prevent cerebral vasospasm (21 days)
  • Hydrate to avoid poor cerebral perfusion & avoid the extremes of BP
  • Control blood pressure
  • Close neuro observation-
    • Hydrocephalus can occur early or later
    • If neuro status deteriorates, urgent head CT required to identify hydrocephalus, which will need a neurosurgical procedure to release the pressure- CSF shunt
188
Q

What are some complications of aneurysmal SAH?

A
  • Re-bleeding
    • Happens in ~10% cases& most common in first 12 hours
    • If rebleeding is suspected (eg sudden worsening of neurological symptoms) then arrange a repeat CT
    • Very high mortality
  • Vasospasm: delayed cerebral ischaemia, typically 1-2 weeks after onset
  • Hyponatraemia (mostly due to SiADH)
  • Seizures
  • Hydrocephalus
  • Death
189
Q

What are some important predictive factors in SAH?

A
  • Conscious level on admission
  • Age
  • Amount of blood visible on CT head
190
Q

What is the normal intracranial pressure?

A
  • 7-15 mmHg in adults in supine position
191
Q

What are the features of a headache due to raised intracranial pressure? What is Cushing’s triad?

A
  • Present on waking
  • May wake them up at night
  • May improve during the day
  • Exacerbated by sneezing, straining, bending, lifting or lying down- all these may further raise the ICP
  • Short hx- days, weeks, few months
  • N&V
  • Effortless vomiting- posterior fossa mass close to 4th ventricle, irritating the vomiting centre
  • Reduced levels of consciousness
  • Cushing’s triad: widening pulse pressure, bradycardia, irregular breathing
192
Q

What are some causes of raised intracranial pressure?

A
  • Idiopathic intracranial hypertension
  • Traumatic head injury
  • Infection- meningitis
  • Tumours
  • Hydrocephalus
193
Q

What is the key Ix for investigating raised ICP?

A
  • CT/ MRI of the brain
  • Invasive ICP monitoring: catheter placed into lateral ventricles of brain to monitor the pressure, may also be used to take samples of CSF and also to drain small amounts of CSF to reduce the pressure
194
Q

What is the management of raised intracranial pressure?

A
  • Ix and treat underlying cause
  • Head elevation to 30 degrees
  • IV mannitol as an osmotic diuretics
  • Controlled hyperventilation
    • Aim is to reduce pCO2 à vasoconstriction of the cerebral arteries à reduced ICP
    • Leads to rapid, temporary lowering of ICP- but caution as may reduce blood flow to already ischaemic parts of the brain
  • Removal of CSF- eg intraventricular monitor, repeated lumbar puncture, ventriculoperitoneal shunt (hydrocephalus)
195
Q

Describe the clinical features and risk factors for benign intracranial hypertension

A
  • Commonly occurs in young, obese women, reproductive age
  • Associated conditions
    • Medications: growth hormones, retinoids
    • Dietary: XS vit A
    • Systemic illness: sleep apnoea, hypercoaguable disorders, PCOS, SLE, Behcet syndrome, endocrine eg Addison’s, hypoparathyroid
  • Signs & symptoms of raised ICP but no mass lesion on CT/ MRI
  • Pathophysiology- impaired CSF absorption
  • Morning headache, vomiting, visual disturbance- diplopia, visual obscurations (sudden, transient bilateral visual loss with changes in posture), tinnitus, bilateral papilloedema, may have 6th nerve palsy & no other focal neurological signs
196
Q

Describe how a diagnosis of benign intracranial hypertension is made and how the condition is subsequently managed

A
  • Clinical features of raised ICP, identification of raised pressures on lumbar puncture, exclusion of alternative cause such as SoL, hydrocephalus, venous sinus thrombosis via neuroimaging g
  • Mx- weight loss, lumbar puncture, may require carbonic anhydrase inhibitor (acetazolamide)
197
Q

What is the temporal artery a branch of?

A
  • The superficial temporal artery is a terminal branch of the external carotid artery
  • It originates at the level of the neck of the mandible
  • After traversing the parotid gland, it runs superficially to the zygomatic process of the temporal bone
198
Q

What is giant cell arteritis?

A
  • A systemic vasculitis of the medium and large arteries
  • Typically affects temporal arteries à temporal arteritis
  • There is a strong link with polymyalgia rheumatica
199
Q

What are the characteristic features of giant cell arteritis (GCA)?

A
  • Unilateral temporal headache
  • Jaw claudication
  • Scalp tenderness
  • Constitutional symptoms- fever, weight loss, fatigue, anorexia, muscle aches
200
Q

Describe how to diagnose GCA?

A
  • When 3 of the following criteria are met-
    • Age of disease onset >50
    • New headache
    • Temporal artery abnormality
    • Elevated ESR (>50mm/hr)
    • Abnormal temporal artery biopsy
201
Q

What is found on a temporal artery biopsy in temporal arteritis?

A
  • Multinucleated giant cells
202
Q

Describe how to manage giant cell arteritis?

A
  • High-dose corticosteroids
    • With visual symptoms: 60-100mg one off prednisolone
    • W/o visual symptoms: 40-60mg daily prednisolone
  • Other medications: aspirin 75mg daily to ↓ visual loss & strokes, and PPI while on steroids (GI protection)
203
Q

What is meningitis?

A
  • Inflammation of the meninges (lining of brain and spinal cord)
  • Neisseria meningitidis- Gneg diplococcus bacteria
204
Q

Describe the clinical features of meningitis?

A
  • Fever
  • Neck stiffness
  • Vomiting
  • Headache
  • Photophobia
  • Altered consciousness
  • Seizures
  • Non-blanching rash (meningococcal septicaemia)
205
Q

What are the special tests that look for meningeal irritation?

A
  • Kernigs test
    • Lying patient on back, flex 1 hip & knee to 90 degrees and then slowly straighten the knee keeping the hip flexed
    • This creates a slight stretch in the meninges and where there is meningitis it will produce spinal pain or resistance to this movement
  • Brudzinski’s test
    • Lying pt flat on back and gently using your hand to lift their head and neck off the bed and flex their chin to chest
    • Positive test: when this causes the pt to involuntarily flex their hips and knees
206
Q

Ix for meningitis?

A
  • FBC, CRP, coagulation screen
  • Blood culture
  • Whole-blood PCR
  • Blood glucose
  • Blood gas
  • If no signs of raised ICP- lumbar puncture
207
Q

Describe the mx of meningitis?

A
  • Community
    • Children with suspected meningitis and non-blanching rash à urgent stat IM or IV benzylpenicillin prior to hospital transfer
  • Hospital
    • Ideally, perform LUP for CSF before starting abx
    • Send bloods for meningococcal PCR
    • < 3 months or >50 years: IV cefotaxime + amoxicillin
    • > 3 months: IV cefotaxime or ceftriaxone
    • Meningococcal meningitis: IV benzylpenicillin or cefotaxime
  • IV dexamethasone given to reduce risk of neurological sequelae and hearing loss
    • Withhold if: septic shock, meningococcal septicaemia, immunocompromised, meningitis following surgery
208
Q

Describe the management of contacts in meningitis pts?

A
  • Prophylaxis to close contacts/ household members, and to those exposed to respiratory secretion regardless of closeness of contact
  • Oral ciprofloxacin or rifampicin
  • Highest risk in first 7 days, persists for 4 weeks
209
Q

Causes of cauda equina syndrome?

A
  • Most common cause central disc prolapse- typically L4/5 or L5/S1
  • Other causes include:
    • Tumours: primary or metastatic
    • Infection: abscess, discitis
    • Trauma
    • Haematoma
210
Q

Clinical features of cauda equina syndrome?

A
  • Lower back pain
  • Bilateral sciatica
  • Reduced sensation/ pins and needles in perianal area
  • Reduced anal tone
  • Urinary incontinence, reduced awareness of bladder filling, loss of urge to void
    • Incontinence is a late sign
211
Q

Ix for CES?

A
  • Urgent MRI
212
Q

How to manage CES?

A
  • Surgical decompression
213
Q

What is acute respiratory distress syndrome?

A
  • Caused by increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli ie non-cardiogenic pulmonary oedema
  • Causes- infection: sepsis, pneumonia, massive blood transfusion, trauma, smoke inhalation, acute pancreatitis, cardio-pulmonary bypass
214
Q

Clinical features of ARDS?

A
  • Dyspnoea
  • Elevated respiratory rate
  • Bilateral lung crackles
  • Low O2 sats
215
Q

Ix for ARDS?

A
  • CXR
  • ABG
216
Q

Mx for ARDS?

A
  • ITU
  • Oxygenation/ ventilation
  • Vasopressors as needed
  • Abx for sepsis
217
Q

Features of Horner’s syndrome?

A
  • Miosis (small pupil)
  • Ptosis
  • Enophthalmos (sunken eye)
  • Anhidrosis (loss of sweating on one side)
218
Q

Causes of subacute combined degeneration of the spinal cord?

A
  • Vitamin B12 deficiency
  • Vitamin E deficiency
  • Copper deficiency
219
Q

Which tracts are affected in SACD?

A
  • Lateral corticospinal tracts
  • Dorsal columns
  • Spinocerebellar tracts
220
Q

How does SACD present?

A
  • Usually affects people > 40
  • Begins w/ general feeling of weakness
  • Tingling, pins & needles, numbness in both hands and feet
  • Constant and gradually worsens
  • Limbs feel stiff, clumsy movements, difficulty to walk
  • Reflexes decreased, increased, or absent
221
Q

How to treat SACD?

A
  • Injections of vitamin B12
222
Q

What is the cavernous sinus?

A
  • One of the (paired) dural venous sinuses of the head
  • Located within the middle cranial fosse, either side of the sella turcica of the sphenoid bone (which contains the pituitary gland)
223
Q

What is cavernous sinus syndrome?

A
  • Caused by any pathology involving the cavernous sinus, may present as a combination of unilateral ophthalmoplegia (CN III, IV, VI), autonomic dysfunction (Horner syndrome) or sensory trigeminal (V1-V2) loss
224
Q

What is a pituitary adenoma and how do they present?

A
  • Benign tumour of pituitary gland
  • 10% of all people- common
  • Most cases never found
  • Most common type: prolactinoma, produce XS prolactin
  • Non-secreting adenomas are the 2nd most common
  • Then GH secreting and ACTH secreting
  • Symptoms caused by excess of hormone: Cushing’s disease due to ACTH, acromegaly due to GH or amenorrhoea and galactorrhoea due to XS prolactin
  • Stretching of the dura within or around pituitary fossa can cause headaches
  • Compression of optic chiasm- causing bitemporal hemianopia due to crossing nasal fibres
225
Q

How to investigate & treat a pituitary tumour?

A
  • Pituitary blood profile: GH, prolactin, ACTH, FH, LSH, TFTs
  • Formal visual field testing
  • MRI brain with contrast
  • Treatment includes a combination of hormonal therapy, surgery and radiotherapy
226
Q

What is Wernicke’s encephalopathy?

A
  • Acute neurological condition
    Triad of ophthalmoparesis with nystagmus, ataxia and confusion
  • Caused by thiamine deficiency which primarily affects the peripheral and central nervous systems
227
Q

What is Argyll Robertson pupil?

A
  • Characterised by small and irregular pupils that have little to no constriction to light but constricts briskly to near targets (light-near dissociation)
  • Pupils are noticeably able to accommodate to near targets
  • Mostly bilateral
228
Q

What disease is Argyll Robertson pupil associated with?

A
  • It is a specific finding in neurosyphilis
229
Q

What is Creutzfeldt-Jacob disease?

A
  • Rapidly progressive neurological condition caused by prion proteins
  • These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases
230
Q

Features of CJD?

A
  • Rapid onset dementia
  • Myoclonus
231
Q

Ix for CJD?

A
  • CSF usually normal
  • EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
  • MRI: hyperintense signals in the basal ganglia and thalamus
232
Q

What are the types of CJD?

A
  • Sporadic
    • 85% all cases
    • Mean age of onset 65
  • New variant CJD
    • Younger pts- 25 years old
    • Psychological symptoms- anxiety, withdrawal, dysphonia
233
Q

What is Syringomyelia and what causes it?

A
  • Syringomyelia describes a collection of CSF within the spinal cord
  • Causes: Chiari malformation, trauma, tumours, idiopathic
234
Q

Features of Syringomyelia?

A
  • Cape like- neck shoulders & arms
    • Loss of sensation to temperature but preservation of light touch, proprioception & vibration
    • Classic examples- burning hands w/o realising
    • This is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected
  • Spastic weakness (predominantly lower limbs)
  • Neuropathic pain
  • Upgoing plantars
  • Autonomic features:
    • Horner’s syndrome due to compression of sympathetic chain (rare)
    • Bowel and bladder dysfunction
  • Scoliosis over years if the syrinx is not treated
235
Q

Ix for suspected syringomyelia?

A
  • Full spine MRI
  • Brain MRI to exclude Chiari malformation
236
Q

Mx for syringomyelia?

A
  • Treat cause of the syrinx
  • Shunt may be placed into the syrinx
237
Q

What is hypoxic ischaemic encephalopathy?

A
  • Type of brain dysfunction that occurs when the brain doesn’t receive enough oxygen or blood flow for a period of time
  • Occurs in neonates during labour

HY Special Senses (3 decks)

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