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Kyla's Phase 2a Flashcards > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the classic triad of Parkinson’s Disease?

A

Resting tremor (rolling pill tremor)
Rigidity (cogwheel rigidity)
Bradykinesia

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2
Q

Who would you suspect PD in?

A

Men above 70 years old

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3
Q

Risk factors for PD

A
  • Increasing age
  • History of familial PD in younger disease
  • Male sex
  • Head trauma
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4
Q

Basic pathology of PD

A

Gradual + progressive fall in dopamine production (from substantia nigra) -> disorders of movement (characteristically asymmetrical)

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5
Q

Key presentations of PD

A

C PUB
C- Cogwheel rigidity
P - Postural instability (stooped posture + forward tilt)
U - Unilateral pill rolling tremor
B - Bradykinesia

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6
Q

How is a diagnosis of PD made?

A

Clinical diagnosis (history and clinical examination)

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7
Q

Differential diagnoses for PD

A

Benign essential tremor
Dementia with Lewy Bodies
Alzheimer’s disease with Parkinsonism
Drug-induced Parkinsonism

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8
Q

Properties of unilateral tremor in PD

A

Asymmetrical
4-6 Hz
Worse at rest
Improves with intentional movement
No change with alcohol

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9
Q

Name some signs of bradykinesia in PD

A

Micrographia
Shuffling gait
Hypomima

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10
Q

When is levodopa prescribed in PD

A

Last line - effectiveness reduces over time

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11
Q

Name a combination drug of levodopa and a peripheral decarboxylase inhibitor used in PD

A

Co-careldopa (levodopa + carbidopa)

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12
Q

Name 3 S/E of levodopa dose being too high

A

Dystonia (abnormal postures or exaggerated movements)
Chorea (abnormal involuntary movements)
Athetosis (involuntary twisting or writhing movements)

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13
Q

Name a COMT inhibitor (used in PD)

A

Entacapone

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14
Q

What are COMT inhibitors used for?

A

In PD - to extend the duration of levodopa

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15
Q

Name a dopamine agonist

A

Bromocryptine
Cabergoline
Pergolide

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16
Q

Name a monoamine oxidase-B inhibitor

A

Selegiline or rasagiline

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17
Q

Complications of PD

A

Levodopa-induced dyskinesia
Dementia
Bladder dysfunction
Orthostatic hypotension
Dysphagia

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18
Q

What type of genetic disease is Huntington’s disease?

A

Autosomal dominant
Also a trinucleotide repeat disorder - anticipation

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19
Q

What is genetic anticipation and what neurological condition displays it?

A

Huntington’s disease
Anticipation = where successive generations have more repeats in the gene -> results in earlier age of onset + increased severity
CAG expansion of the first exon in the Huntingtin gene (HTT)

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20
Q

When does Huntington’s present in life?

A

Typically mid-life
(But can be any age)

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21
Q

What are the earlier symptoms of Huntington’s

A

Cognitive, psychiatric and mood problems (personality change, irritability and impulsivity)

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22
Q

What are the signs of Huntington’s

A

Chorea (involuntary abnormal movements)
Eye movement disorders (slowed rapid eye movements)
Dysarthria (speech difficulties)
Dysphagia (swallowing difficulties)
Loss of coordination
Deficit in fine motor coordination

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23
Q

Testing for Huntington’s

A
  • CAG repeat testing
  • Rest is clinical
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24
Q

What is the treatment for slowing or stopping the progression of Huntington’s?

A

None - just supportive

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25
Q

Management for Huntington’s disease

A

Speech and language therapy
Genetic counselling
End of life care planning
Antidepressants for depression

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26
Q

Two main complications of Huntington’s disease

A

Depression -> suicide
Dysphagia -> aspiration pneumonia

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27
Q

Typical life expectance after the onset of Huntington’s disease?

A

15-20 years after symptom onset
Death due to aspiration pneumonia + suicide

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28
Q

Define MS

A

T-cell mediated inflammatory demyelinating disorder of the CNS - characterised by the presence of episodic neurological dysfunction in at least 2 areas of the CNS (brain, spinal cord, optic nerves - separated in time and space

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29
Q

What individual are you most likely to diagnose MS in?

A

Females under 50
(disease of the young)
Effects x2 women

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30
Q

Causes of MS

A
  • Multiple genes (polygenic)
  • EBV
  • Low vitamin D
  • Smoking
  • Obesity
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31
Q

What type of hypersensitivity reaction underpins MS pathology?

A

Type IV (cell-mediated)

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32
Q

Very basic MS pathology

A

T-cell mediated
T cells = activate B cells to produce auto-antibodies against myelin -> demyelination -> disruption of conduction along axon

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33
Q

What does ‘disseminated in time and space mean in MS?

A

Key characteristic in MS
Lesions vary in their location over time
Therefore symptoms change over time

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34
Q

What is Uhtoff’s phenomenon in MS

A

Worsening of neurological symptoms in MS when the body gets overheated

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35
Q

Name a clinical sign in MS examination

Involves the neck

A

Lhermitte’s sign
Bending neck forward -> electric shock runs down back -> radiates to limbs

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36
Q

Name the group of symptoms in MS

A
  • Optic neuritis (loss of vision in one eye)
  • Eye movement abnormalities (double vision)
  • Focal weakness (e.g. limb paralysis or incontinence)
  • Focal sesnory symptoms (e.g. numbness, paraesthesia, Lhermitte’s sign)
  • Ataxia (sensory or cerebellular)
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37
Q

Name the disease patterns of MS (4)

A
  • Clinically isolated syndrome
  • Primary progressive MS
  • Relapsing-remitting MS
  • Secondary progressive MS
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38
Q

Investigations for MS

A
  • MRI brain and spinal cord (demonstrate demyelinating lesions) - first line
  • Lumbar puncture (‘oligoclonal bands’ in CSF)
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39
Q

3 Differential diagnoses for MS

A

Fibromyalgia
Sjorgren syndome
Vitamin B12 deficiency
Peripgeral neuropathy
Amyotrophic lateral sclerosis (ALS)

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40
Q

Management for MS

A
  • Immunomodulators (interferon beta 1a (IM) or 1b (SC)) + rituximab
  • Relapses - IV methylprednisolone
  • Symptomatic treatments (neuropathic pain - amitriptyline or ganapentin, spasticity - gabapentin)
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41
Q

Complications of MS

A
  • Depression
  • Visual impairment
  • Erectile dysfunction
  • Cognitive impairment
  • Impaired mobility
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42
Q

Lesions in which cranial nerve cause double vision in MS?

A

CN VI (abducens)
(Sixth cranial nerve palsy -> muscles around eye cannot move eye laterally)

MS - Sixth cranial nerve

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43
Q

Define epilepsy

A

Umbrella term for a condition where there is a tendency to have seizures

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44
Q

Define seizure

A

Transient episodes of abnormal electrical activity in the brain

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45
Q

What type of seizures present as a loss of consciousness + tonic (muscle tensing) + clonic (muscle jerking) episodes?

A

Generalised tonic-clonic seizure

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46
Q

What might the patient do in a tonic-clonic seizure?

A
  • Tongue-bitting
  • Groaning
  • Irregular breathing
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47
Q

What is a post-ictal period?

A

Occurs after a seizure
Patient becomes confused, drowsy, irritable or depressed

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48
Q

First and second line management for a generalised tonic-clonic seizure

A
  • First line: Sodium valproate
  • Second line: Carbamazepine or Lamotrigine
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49
Q

What region of the brain do focal sezuires begin in?

A

Temporal lobes

Focal seizures affect hearing, speech, memory, emotions

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50
Q

A patient has seizures and experiences:
* Hallucinations
* Memory flashbacks
* Deja vu
* Doing strange things on autopilot
What type of seizure are they experiencing?

A

Focal seizure

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51
Q

What is the first line and second management for focal seizures?

A
  • First line: Carbamazepine or Lamotrigine
  • Second line: Sodium valproate
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52
Q

Name 2 investigations for epilepsy

A
  • Electroencephalogram (EEG)
  • MRI brain (diagnose structural pathology)
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53
Q

Differential diagnoses for seizures
DRIFT 3R

A
  • Drugs
  • Rum (alcohol withdrawal)
  • Illness (chronic)
  • Fever
  • Trauma
  • 3 antis (antihistamine, anticonvulsants, antidepressants)
  • Rat poison
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54
Q

Name an important contraindication for sodium valproate

A

Teratogenic
Avoid in pregancy and young women!

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55
Q

Why do you have to be carreful when prescribing carbamazepine?

A

Many drug interactions!
(It induces the P450 system)

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56
Q

What is status epilepticus?

A
  • Continuous seizure for more than 5 mins
    OR
  • 3 seizures in 1 hour
    MEDICAL EMERGENCY
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57
Q

Complications of status epilepticus

A

Permanent brain damage -> death

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58
Q

Treatment of status epilepticus in hospital and the community

A
  • Hospital: ABCDE approach + IV lorazopam
  • Community: Rectual diazepam
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59
Q

Define Guillian-Barre syndrome

A

An acute paralytic neuropathy - that affects the peripheral nervous system

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60
Q

What key symptoms does Guillian-Barre syndrome produce?

A

Acute, symmetrical ascending weakness
Also may cause sensory problems

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61
Q

Name 3 main triggers for Guillian-Barre syndrome

A
  • Camplyobacter jejuni
  • EBV
  • CMV
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62
Q

What is the key term that underpins Guillan-Barre pathophysiology?

A

MOLECULAR MIMICRY
B-cells produce antibodies that target the myelin sheath and axon of motor nerve cells

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63
Q

A patient presents with:
* Symmetrical ascending weakness (starting at feet, moves up)
* Reduced relexes
* Neuropathic pain
* Peripheral loss of sensation
* Facial nerve weakness
Suspected diagnosis?

A

Guillian-Barre syndrome

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64
Q

What is the key presentation of Guillian-Barre syndrome?

A

Symmetrical ascending weakness (starting at feet - moves up the body)

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65
Q

A patient presents with gastritis and within 4 weeks complains of loss of sensation and neuropathic pain in feet. Diagnosis?

A

Guillian-Barre syndrome

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66
Q

What are 2 confirmatory tests for Guillian-Barre syndrome?

A
  • Nerve conduction studies (reduced signal through the nerves)
  • Lumbar puncture (elevated CSF proteins)
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67
Q

What is the management for Guillian-Barre syndrome

A
  • IV immunoglobulins (IVIG)
  • Plasma exchange (alternative to IVIG)
  • Supportive care
  • VTE prophylaxis (DOAC, LMWH)
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68
Q

Name a couple of complications of Guillian-Barre Syndrome

A
  • Respiratory failure
  • Paralysis
  • DVT
  • Fatigue
  • Psychological problems
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69
Q

The Brighton criteria is used to diagnose which neurological condition?

A

Guillian-Barre syndrome

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70
Q

Patient presents with a mild ache across forehead (band-like headache pattern around the headache). Normal neurological examination and NO associated features N+V. Diagnosis?

A

Tension headache

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71
Q

Name some causes of a tension headache

A
  • Stress
  • Missing meals
  • Dehydration
  • Alcohol
  • Depression, anxiety
  • Eyestrain
  • Noise
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72
Q

Which muscles are thought to cause ache in a tension headache?

A
  • Frontalis
  • Temporalis
  • Occipitalis
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73
Q

Describe the characteristic features of a tension headache

A

Dull, non-pulsatile, bilateral constricting pain

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74
Q

Differentials for a tension headache

A
  • Chronic migraine
  • Giant cell arteritis
  • Brain tumour
  • Pituitary tumour
  • Medicine overuse headache
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75
Q

Possible complication of a tension headache

A

Peptic ulcer
(secondary ulcer to NSAID use)

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76
Q

Define migraine

A

Complex neurological condition that causes headache + other associated symptoms

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77
Q

Types of migraine

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (aura with no headache)
  • Hemiplegic migraine (temporary weakness on one side of the body)
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78
Q

How long does a migraine typically last?

A

4 to 72 hours

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79
Q

Patient presents with a unilateral pounding or throbbing headache with nausea and vomiting, and a discomfort to lights and loud noises. All investigations come back normal. Diagnosis?

A

Migraine

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80
Q

Symptoms of a migraine

A
  • Moderate-to-severe intensity
  • Pounding or throbbing in nature
  • Usually unilateral - but can be bilateral
  • Photophobia (discomfort with lights)
  • Phonophobia (discomfort with loud noises)
  • Aura - with or without
  • Nausea + vomiting
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81
Q

Patient presents with sparks and blurring of vision followed by a headache. All investigations come back normal. Diagnosis?

A

Migraine with aura

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82
Q

What is aura?

A

Visual changes associated with migraines
* Sparks in vision
* Blurring in vision
* Lines across vision
* Loss of different visual fields

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83
Q

Patient presents with unilateral weakness in limbs, ataxia and a throbbing painful sensation in head. There are aslo changes in conscious. CT head comes back normal . Diagnosis?

A

Hemiplegic migraine

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84
Q

Name the 5 stages of a migraine

A
  • Prodromal
  • Aura
  • Headache
  • Resolution
  • Postdromal
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85
Q

Differentials for a migraine

A
  • Tension headache
  • Cluster headache
  • Medication-overuse headache
  • Subarachnoid haemorrhage (SAH)
  • Giant cell arteritis
  • Headache after head or neck trauma
  • Stroke (if hemiplegic migraine)
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86
Q

Name the 3 drug classes used in the first line management of a migraine

A
  • Analgesics
  • Triptans
  • Antiemetics
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87
Q

What is sumatriptan and when is it used?

A

A triptan - used in migraine

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88
Q

What is metoclopramide used for?

A

An antiemetic

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89
Q

What is promethazine

A

An antiemetic (antihistamine)

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90
Q

Name some migraine prophylaxis used to reduce frequency + severity of attacks

A
  • Propanolol
  • Topiramate
  • Amitryptyline
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91
Q

Complications of a migraine

A
  • Depression
  • Complications of pregnancy
  • Chronic migraine
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92
Q

Key medication for a migraine

A

Triptans
E.g sumatriptan

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93
Q

Describe the presentation of a cluster headache

A

Severe unbearable unilateral headaches around one eye

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94
Q

Typical person to present with a cluster headache

A

50 y/o male smoker

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95
Q

Patient presents with:
* Read, swollen watering eye
* Miosis (pupil constriction)
* Ptosis (Eye drooping)
* Nasal discharge
* Headache around one eye
All investigations come back normal. Diagnosis?

A

Cluster headache

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96
Q

First line investigations for a cluster headache

A
  • MRI brain (normal)
  • ESR (normal)
  • Pituitary function tests (normal)
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97
Q

Differentials for a cluster headaches

A
  • Migraine
  • Trigmenial neuralgia
  • Subarachnoid haemorrhage
  • Giant cell arteritis
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98
Q

What is the acute management for a cluster headache?

A
  • Triptans (sumatriptan injected s/c)
  • High flow 100% oxygen
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99
Q

Second line management for a cluster headache

A
  • Intranasal zolmitriptan
  • Intranasal lidocaine
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100
Q

Cluster headache prophylaxis

A
  • Verapamil
  • Lithiuum
  • Prednisolone
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101
Q

Complications of cluster headaches

A

Depression

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102
Q

What condition involves an intense stabbing paroxysmal pain in the trigeminal nerve (CN V)?

A

Trigeminal neuralgia

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103
Q

Main cause of trigeminal neuralgia

A

Vein or artery compressing the trigeminal nerve
Other causes:
- Local pathology pressing on trigeminal nerve (more common in younger people)
- Aneurysms
- Meningeal inflammation
- Tumours - vestibular schwannoma
- 5th nerve lesion
- Brainstem → tumour, MS, infarction
- Cerebellopontine angle – acoustic neuroma, other tumour

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104
Q

Risk factors for trigeminal neuralgia

A
  • Multiple sclerosis (demyelinating disorder)
  • Increased age
  • Female sex
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105
Q

Pathophysiologiy of trigeminal neuralgia

A

Compression of the trigeminal nerve -> results in demyelination + excitation -> erratic pain signalling

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106
Q

What can trigger an attack of trigeminal neuralgia?

A

Facial or oral mechanical stimulation. E.g.:
* Touching/moving tongue
* Chewing
* Brushing teeth
* Blowing nose
* Hot/cold drinks

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107
Q

Describe the pain involved in trigeminal neuralgia

A
  • Recovering paroxysmal attacks
  • Severe intensity
    ** Sharp, stabbing, shooting, electric shock
    **     Usually unilateral
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108
Q

Investigations for trigeminal neuralgia

A

First line: clinical diagnosis Other:
* MRI
* Trigeminal reflex testing
* Intra-oral x-ray

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109
Q

Differentials for trigeminal neuralgia

A
  • Dental caries
  • Dental fracture
  • Migraine
  • Temporal arteritis
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110
Q

Management for trigeminal neuralgia

A
  • First line: Carbamazepine orally
  • Second line: Phenytoin, gabapentin
  • Microvascular decompression
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111
Q

Define myasthenia gravis

A

Autoimmune condition that causes skeletal weakness

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112
Q

What disease is linked to myasthenia gravis

A

Thymoma

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113
Q

What type of hypersensitivity reaction underpins myasthenia gravis?

A

Type II hypersensitivity reaction

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114
Q

Pathology that underpins myasthenia gravis

A

Ach receptor antibodies = bind to post-synaptic neuromuscular junction receptors
Blocks the receptor -> ACh is unable to stimulate the receptor -> cannot trigger muscle contraction

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115
Q

Antibodies involved in myasthenia gravis

A
  • ACh receptors
  • Muscle-specific kinase (MuSK)
  • Low-density lipoprotein receptor-related protein (LRP4)
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116
Q

When does myasthenia gravis improve and worsen?

A
  • Worsens with activity
  • Improves with rest
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117
Q

Symptoms of mysathenia gravis

A

The symptoms most affect theproximal musclesand small muscles of the head and neck. It leads to:

  • Extraocular muscle weakness causing double vision (diplopia)
  • Eyelid weakness causing drooping of the eyelids (ptosis)
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
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118
Q

Examination of myastheia gravis

A

Elicit atiguability in the muscles:
* Repeated blinking
* Prolonged upward gazing
* Repeated abduction of one arm 20 times

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119
Q

First line investigations for myasthenia gravis

A
  • Serum ACh receptor antibody analysis
  • Muscle-specific tyrosine kinase (MuSK) antibodies
  • Low-density lipoprotein receptor-related protein (LRP4)
  • Serial pulmonary function tests (FVC + NIF)
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120
Q

When is the edrophonium test performed?

A

Diagnosis of myasthenia gravis

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121
Q

First-line treatment of myasthenia gravis

A
  • Neostigmine or pyridostigmine
  • Prednisolone or azathioprine
  • Rituximab
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122
Q

Management of myasthenic crisis

A
  • Non-invasive ventilation
  • Full intubation + ventilation
  • Immunomodulatory therapies (IV immunoglobulins, plasma exchange)
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123
Q

Which head presents as a dull, non-pulsatile, bilateral constricting pain (not severe, like a band around their head)?

A

Tension headache

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124
Q

How does a migraine persent?

A
  • Moderate-to-severe intensity
  • Pounding or throbbing
  • Usually unilateral
  • Photophobia or phonophobia
  • Can be preceeded by aura
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125
Q

What is aura?

A

Visual changes associated with migraines
* Sparks in vision
* Blurring in vision
* Lines across vision
* Loss of different visual fields

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126
Q

Patient presents with unilateral throbbing headache, unilateral weakness of the limbs, ataxia and changes in conscious

A

Hemiplegic migraine
(can mimic a stroke)

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127
Q

Name some prodromal stage symptoms of a migraine

A

Yawning, fatigue, mood changes, followed by aura

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128
Q

First line management for a migraine

A
  • NSAID
  • Antiemetic (metaclopramide)
  • Triptans (sumatriptan) - in severe cases
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129
Q

When do you use triptans?

A

As migraine starts
(e.g. sumatriptan)

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130
Q

Name 3 drugs used in migraine prophylaxis

A
  • Propanolol
  • Amitriptyline
  • Topiramate (teratogenic)
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131
Q

What trigger in women may trigger a migraine?

A

Menstrual cycle
(may warrant prophylaxis)

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132
Q

Name some acute diagnosis differents of a migraine

A
  • Subarachnoid haemorrhage (SAH) (CT)
  • Giant cell arteritis (jaw claudication, inflammatory markers)
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133
Q

What headache can be described as a ‘suicide headache’?

A

Cluster headache
(suicide = a complication)

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134
Q

Typical patient to present with a cluster headache?

A

30-50 year old male smoker

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135
Q

Describe the symptoms of a cluster headache

A

One-sided sharp, stabbing, burning, orbital/supraorbital, temporal head pain

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136
Q

Describe the signs of a cluster headache

A
  • Red swollen, watering eye
  • Pupil constriction (miosis)
  • Eye drooping (ptosis)
  • Nasal discharge
  • Facial sweating
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137
Q

First line investigations for a cluster headache

A
  • MRI brain (with contrast) (normal)
  • ESR (normal)
  • Pituitary function tests (normal)
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138
Q

One clinical exam to perform on a patient with a headache

A

Fundoscopy
(check for papilloedema - rasied intracranial pressure)

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139
Q

Complications for headaches

A

Depression!

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140
Q

Most common cause of trigeminal neuraglia

A

Vein or artery compressing the trigeminal nerve
(Results in demyelination + excitation -> results in erratic pain)

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141
Q

Triggers for trigeminal neuralgia attacks

A

Facial or oral mechanical stimulation
* Touching/moving tongue, lips, face
* Chewing
* Shaving
* Brushing teeth
* Blowing nose
* Hot/cold drinks

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142
Q

Patient presents with severe sharp, stabbing, shooting, electric shock pain in face, usually unilateral. Occurs in more than one distribution of the trigeminal nerve. Recovering paroxysmal attacks (1s-2min)

A

Trigeminal neuralgia

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143
Q

A sign of trigeminal neuralgia

A

Facial muscle spasms/autonomic symptoms

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144
Q

Differential diagnoses of trigeminal neuralgia

A
  • Dental caries
  • Dental fracture
  • Migraine
  • Temporal arteritis
  • Mandibular osteomyelitis
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145
Q

First line and second line management of trigeminal neuralgia

A
  • First line: Carbamazepine
  • Second line: Phenytoin, gabapentin (analgesic targeted for neuropathic pain)
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146
Q

Surgical interventions for trigeminal neuralgia

A
  • Microvascular decompression
  • Ablative surgery
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147
Q

Define epilepsy and a seizure

A
  • Epilepsy = umbrella term to describe when there is a tendency to have seizures
  • Seizure = transient episodes of abnormal brain activity
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148
Q

Name some seizures

A
  • Generalised tonic-clonic
  • Focal
  • Absence
  • Atonic
  • Myoclonic
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149
Q

Patient has a loss of conscious with muscle tensing and jerking. They also bite their tongue, wet themselves, and are breathing irregularly. Diagnosis?

A

Generalised tonic-clonic seizure

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150
Q

What is a post-ictal period?

A

Period after a seizure, presents confused, drowsy, irritable or depressed

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151
Q

First and second line management for a generalised tonic-clonic seizure

A
  • Sodium valproate
  • Lamotrigine or carbamazepine
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152
Q

Where do focal seizures start in the brain?

A

Temporal lobes

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153
Q

Differences between a focal aware seizure and a focal impaired awareness seizure

A
  • Focal aware seizure = consciousness preserved
  • Focal impaired awareness seizures = loss of awareness, memory loss of seizure, impaired responsieness during seizure
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154
Q

What can a focal seizure evolve into?

A

bilateral tonic-clonic seizure
(formally known as secondary generalised tonic-clonic seizure)

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155
Q

Patient presents with a sense of deja vu and then hallucinates. Their hearing and speech are also affected. Diagnosis?

A

Focal seizure

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156
Q

Management for a focal seizure?

A
  • First line: Carbamazepine or lamotrigine
  • Second line: sodium valproate
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157
Q

Difference between management of a focal seizure and a generalised tonic-clonic seizure

A

The first line and second line are swapped

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158
Q

A child randomally becomes blank, stares into space, then abruptly returns to normal (unaware of surroundings) - lasting 10-20s

A

Absence seizure

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159
Q

First line management of an absence seizure

A

Sodium valproate or ethosuximide

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160
Q

A child randomly drops to the floor and is there for less than 3 minutes. Diagnosis?

A

Atonic seizure

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161
Q

Management foran atonic seizure

A
  • First line: sodium valproate
  • Second line: Lamotrigine
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162
Q

A patient suddenly has brief muscle contractions (like a ‘suden jump’) - they remain awake during the episode. Diagnosis?

A

Myoclonic seizure

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163
Q

First and second line management for myoclonic seizures

A
  • First line: Sodium valproate
  • Second line: Lamotrigine
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164
Q

Diagnosis of epilepsy requirements

A

At least 2 unprovoked seizures occurring 24 hours apart

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165
Q

Investigations for epilepsy

A
  • Clinical examination + history
  • Electroencephalogram (EEG)
  • MRI brain
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166
Q

Differential diagnoses for epilepsy

A

DRIFT 3R
* Drugs
* Rum (alcohol withdrawal)
* Illness (chronic)
* Fever
* Trauma
* Antis
* Rat poison

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167
Q

A female of child-bearing age with epilspsy needs to be prescribed medication, which one are you going to avoid?

A

Sodium valproate
(Highly teratogenic)

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168
Q

Side effects for carbamazepine

A
  • Aplastic anaemia
  • Induces the P450 system (so many drug interactions
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169
Q

What is status epilepticus?

A

Continuous seizure activity for over 5 mins -> permanent brain damage -> death

Or 3 seizures in an hour

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170
Q

How do you treat status epilepticus in the community and hospital?

A
  • Community: Buccal midazolam
  • Hospital: IV lorazepam (then IV phenytoin or IV phenobarbital if persists)
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171
Q

Progression of brain atrophy in AD

A

Medial temporal lobe -> limbic system -> widespread throughout brain

172
Q

Describe the onset of AD

A

Insidious, progresses steadily
(deteriorating course over 8-10 years)

173
Q

Describe the early, intermediate and advanced stages of AD

A
  • Early: Recent memory impairment, impaired reasoning, concentration loss, sleep disturbance
  • Intermediate: Behavioural psychological symptoms, motor task completion difficulties
  • Advanced: Complete debilitation (urinary/faecal incontinence)
174
Q

First line investigations for AD

A
  • Mini Mental State Examination
  • MRI head (generalised atrophy with medial temporal lobe)
175
Q

Differential diagnoses for AD

A
  • Delirium
  • Depression
  • Vascular dementia
  • Dementia with Lewy bodies
  • Frontotemporal dementia
  • Parkinson’s disease dementia
176
Q

First line management for AD

A
  • Cholinesterase inhibitor (oral rivastigmine or donepezil)
  • Anti-glutamate (memantine)
177
Q

Name a cholinesterase inhibitor

A
  • Rivastigmine
  • Donepezil
178
Q

Define Alzheimer’s disease

A

Alzheimer’s disease (AD) is a chronic, progressive neurodegenerative disorder characterised by a global, non-reversible impairment in cerebral functioning.

179
Q

Which lobes area affected in frontotemporal dementia?

A
  • Frontal
  • Temporal
180
Q

How does frontotemporal dementia usually present?

A
  • Disruption in personality + social conduct
    OR
  • Primary language disorder
181
Q

What do 50% of people with frontotemporal dementia also display?

A

Parkinsonism

182
Q

When is the typical onset of frontotemporal dementia?

A

45-65 years

183
Q

What specifc-protein cellular inclusions are involved in frontotemporal dementia?

A

Tau protein build-up → stop neuronal signalling → neuron apoptosis

184
Q

What genetic mutation is a risk factor for frontotemporal dementia?

A

MAPT gene

185
Q

What two types of motor disease are associated with frontotemporal dementia?

A
  • Parkinsonism
  • Motor neuron disease
186
Q

What are the signs and symptoms of frontotemporal lobe dementia?

A
  • Frontal lobe involvement →behaviour/emotional changes
    • Disinhibition, emotional blunting, apathy/empathy-loss, compulsive behaviour, family/friend dissociation (argumentative/hostile behaviour)
  • Temporal lobe involvement → language impairment, emotional disturbance
    • Difficulty finding correct word, progressive aphasia, impaired word comprehension
  • Later stages → cognitive decline
    • Worsening memory, inability to learn new things, concentration loss
187
Q

A patient presents with:
* Changes in personality and social behaviour
* Progressive loss of language comprehension
* Memory impairment, disorientation, apraxia
* Self-neglect and abandonment of social activity and contacts

Possible diagnosis?

A

Frontotemporal dementia

188
Q

What are the Ix for frontotemporal dementia?

A
  • Formal cognitive testing
    • Frontotemporal rating scale (FRS)
    • MMSE (not great)
  • Brain MRI
    • Atrophy in the front and/or anterior temporal lobes
    • (usually left-right asymmetry)
189
Q

When investigating frontotemporal dementia, if a brain MRI becomes back normal or intermediate. What imaging should you request? What would it show if positive?

A

Brain fluorodeoxyglucose (FDG-PET) scan
* Focal hypo-metabolism in the frontal and/or anterior temporal lobes (frequently asymmetrical)

190
Q

What is the non-pharmacological and pharmacological treatments of frontotemporal dementia?

A

Non-pharmacological:
* Physical exercise
* Occupational therapy
* Increased supervision

Pharmacological:
* Benzodiazepine or antipsychotoc (lorazepam, risperidone)
* SSRI (citalopram or sertraline)
* Trazodone (sleep disturbances)

191
Q

Possible complications for frontotemporal dementia

A
  • Irresponsible/compulsive spending
  • Dangerous driving
  • Falls
  • Problems with family relationships
192
Q

What protein is responsible for Lewy body dementia and where is it found?

A
  • Alpha-synuclein protein aggregation → Lewy bodies → apoptosis
  • Cortex + substantia nigra
193
Q

What are the key presentation of Lewy Body dementia?

A
  • Cognitive impairment
    • Attention, executive, visuospatial functions, memory (later)
  • Visual hallucinations, disordered speech
  • Parkinsonism
    • Resting tremor
    • Stiffness, slow movement
    • Reduced facial expressions
  • REM sleep behavioural disturbance
194
Q

Imaging for Lewy body dementia. What does it show?

A
  • CT/MRI head
  • Generalised cortical atrophy
    (preservation of the medial temporal lobe (particularly the hippocampus)
  • CT PET
195
Q

What are the first and second line treatments for Lewy Body dementia?

A

First line:
* Supportive care
* Cholinesterase inhibitor (rivastigmine or donepezil)
* SSRIs (sertraline or citalopram)
* Sleep disturbance → clonazepam
* Severe motor symptoms → dopaminergic agent (carbidopa/levodopa)

Second line:
* Memantine (orally)
* Antipsychotic (risperidone)

196
Q

Name an antipsychotic

A

Risperidone

197
Q

Name a cholinestarse inhibitor

A
  • Rivastigmine
  • Donepezil
198
Q

Complications of Lewy Body dementia

A
  • (Aspiration) Pneumonia
  • Dysphagia
  • Antipsychotic sensitivity
  • Urinary incontinence
  • Falls
199
Q

What drug is effective for REM sleep behavioural disorder in Lewy body dementia?

A

Clonazepam

200
Q

What are some causes of vascular dementia?

A

Cerebrovascular changes: E.g. Infarction, haemorrhage
* Cerebral artery atherosclerosis
* Carotid artery/heart embolisation
* Chronic hypertension → cerebral arterioles sclerosis
* Vasculitis

201
Q

Name a couple of Rx for vascular dementia

A
  • Age > 60 yrs
  • Obesity
  • Hypertension
  • Cigarette smoking
202
Q

Where does the damage occur in vascular dementia?

A

Grey + white matter

203
Q

What are the key presentations of vascular dementia?

A
  • Prominent executive function deficit
    • Progressive stepwise cognitive function impairment
  • Late-onset memory impairment
204
Q

What does damage in the frontal lobe lead to?

A

Executive dysfunction

205
Q

What does damage in the left parietal lobe lead to?

A
  • Aphasia
  • Apraxia
  • Agnosia
206
Q

What does damage in the right parietal lobe lead to?

A
  • Hemineglect (unaware of one side of body)
  • Confusion
  • Agitation
  • Visuospatial difficulty
207
Q

What does damage in the temporal lobe do?

A

Anterograde amnesia

208
Q

Ix for vascular dementia

A
  • Brain CT/MRI
    • Cerebrovascular lesions (multiple cortical, subcortical infarcts)
  • ECG (AF may be present)
  • Vitamin B12 (rule out for cognitive decline)
  • Carotid duplex/doppler ultrasound (reveal carotid plaques/carotid stenosis)
  • Echocardiogram (reveal cardiogenic emboli)
209
Q

What is the management for vascular dementia?

A
  • Antiplatelet therapy (prevent further infarction)
    • Aspirin or clopidogrel (orally)
  • Lifestyle modification
  • Concomitant AD → Memantine OR acetylcholinesterase inhibitor (donepezil or rivastigmine)
  • Vadcular risk factor control (atorvastatin)
  • Depression/agitation (sertraline)
210
Q

How is vascular dementia characterised?

A

Chronic progressive multifaceted impairment of cognitive function

211
Q

Descrbe the onset of a stroke

A

SUDDEN ONSET

212
Q

Define an ischaemic stroke?

A
  • Neurological dysfunction
  • Caused by focal cerebral, spinal or retinal infarction
  • (Cell death due to lack of blood supply)
213
Q

What are the 5 types of ischaemic stroke? (Classification)

A

TOAST Classification
- Large artery atherosclerosis
- Small artery strokes
- Cardioembolic infarction
- Formation of emboli in heart → lodging in brain arteries
- AF, MI, IE
- Other determined pathology
- Undetermined pathology

214
Q

What proportion of strokes are ischaemic?

A

80%

215
Q

Name some causes of ischaemic stroke

A
  • Large artery stemosis
  • Cardioembolic (AF, MI, IE)
  • Atherothromboembolism (e.g. from cartotid artery)
  • Shock (reduced blood flow throughout body)
  • Vasculitis
216
Q

Rx for iscahemic stoke

A
  • Older age (esp. >55)
  • Hypertension
  • Smoking
  • Male sex
  • Same risk factors as atherosclerosis → atherosclerotic plaque → occlusion of cerebral artery → ischaemic stroke
217
Q

Pathophysiology of an ischaemic stroke

A
  • Blood vessel occlusion → decreased blood supply in specific brain area → hypoperfusion → tissue hypoxia → infarction
  • ↓blood flow → ↓oxygen + glucose in brain → ↓ATP production → cell death
218
Q

Pathology of thrombosis in ischaemic stroke

A
  • Obstruction in blood vessel
  • Narowing of blood vessel due to atherosclerotic plaque → gradual reduced blood flow
  • Damage to atherosclerotic fibrous cap → platelet + clotting cascade activation → thrombus formation with sudden stop to blood flow
219
Q

Key generalised presentations of an ischaemic stroke

A
  • Unilateral weakness or paralysis in face, arm, leg
  • Dysphasia (difficulty in speech - slurred)
  • Ataxia
  • Visual disturbance
220
Q

What is the scoring system for assessing the risk of an ischaemic stroke?

A

ABCD2
* A - Age
* B - Blood pressure
* C - Clincial presentation
* D - Duration of symptoms
* D - Diabetes

221
Q

First line and other Ix for ischaemic stroke

A

First line:
* CT head (no contrast)
* Blood (exclude hypoglycaemia)
* ECG +/- hour tape
- AF or MI

Gold-standard:
* Diffusion-weighted MRI head (more sensitive)

Other:
* Carotid doppler
* Echo
* CT or MRI angiogram

222
Q

What is the first line treatment for an ischaemic stroke?

A

Within 4.5 hours:
* Thrombolysis (IV altepase)

Within 6-24 hours:
* Thrombectomy (mechanical removal of clot)

BP should not be lowered during stroke - risk reducing perfusion

223
Q

What does ROSIER stand for and when is it used?

A

Recognition of Stroke in the Emergency Room

224
Q

4 potential mechaisms for ischaemic stroke

A
  • Embolism: an embolus originating somewhere else in the body (e.g. the heart) causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of the brain the vessel supplies.
  • Thrombosis: a blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
  • Systemic hypoperfusion: blood supply to the entire brain is reduced secondary to systemic hypotension (e.g. cardiac arrest).
  • ** Cerebral venous sinus thrombosis**: blood clots form in the veins that drain the brain, resulting in venous congestion and tissue hypoxia.
225
Q

Which regions of te brain are supplied by the anterior cerebral arteries?

A

Anteromedial area of cerebrum

226
Q

Which region of the brain is supplied by the middle cerebral arteries?

A

Lateral cerebrum

227
Q

Which regions of the brain are supplied by the posterior cerebral arteries?

A

Posterior cerebrum

228
Q

Based on the initial presenting symptoms + clinical signs - what classification system is used in ischaemic stroke?

A

Bamford classification

229
Q

What are the principal management of an intracranial bleeds?

A
  • ** Immediate CT head to establish the diagnosis
  • Check FBC and clotting
  • Admit to a specialist stroke unit**
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
    *
230
Q

What is an intracerebral haemorrhage?

A
  • Blood vessels rupture → intraparenchymalblood accumulation
231
Q

Pathology of an intracerebral haemorrhage

A

Blood vessel trauma → rupture → creates blood of blood → tissue + surrounding blood vessel compression → hypoxia in downstream tissue → damage due to compression → oxygen lack

232
Q

Causes of intracerebral haemorrhage

A
  • Hypertension (most common)
  • Atherosclerosis
  • Vascular abnormalities
    • Cerebral amyloid angiopathy
    • Vasculitis
  • Secondary to ischaemic stroke
    • Blood flow blockage → reperfusion → increased chance of blood vessel rupture → bleeding into dead tissue
233
Q

Rx for intracerebral haemorrhage

A
  • Male sex
  • Black individuals (African descent)
  • Heavy alcohol use, amphetamines, cocaine abuse, antithrombotic medications
234
Q

General presentation of an intracranial haemorrhage

A
  • Begin slowly → worsen gradually
  • Enlargement of haematoma (within few hours) → increased intracranial pressure
    • Altered consciousness
    • Headache
    • Nausea + vomiting
    • Unequal pupil size
235
Q

Sx if there a stroke in the anterior/middle cerebral artery

A

Numbness + sudden muscle weakness

236
Q

Sx if there a stroke in the posterior cerebral artery

A

Impaired vision

237
Q

Sx if there a stroke in Broca’s area

A

Slurred speech

238
Q

Sx if there a stroke in Wernicke’s area

A

Difficulty understanding speech

239
Q

What is a major complication of intracerebral haemorrhage?

A

Hydrocephalus

240
Q

Ix for intracerebral haemorhage

A
  • Head CT (no contrast)
    • Trauma → multifocal bleedings
  • CT angiography
    • Unifocal/multifocal enhancement of contrast
  • Diffusion-weighted MRI (T2-WI)
  • Bloods:
    • Prothrombin time
    • FBC (platelet count)
241
Q

Treatment of intracerebral haemorrhage

Not sure on this

A
  • With anticoagulant usage → Vitamin K, unactivated prothrombin
  • Enalapiril (hypertension)
  • Phenytoin (seizures)
  • Antipyretics (fever reduction)

Surgery:
- If haemorrhage >3cm / brainstem compression
- Craniotomy with clot removal
- Endoscopic evacuation

242
Q

If a patient presents with a thnderclap headache, what is the main worrying possible diagnosis?

A

Subarachnoid haemorrhage

243
Q

Where does a subarachnoid haemorrhage occur?

A

Between the pia mater + arachnoid mater
(In the subarachnoid space)

244
Q

Pathology of a spontaneous haemorrhage

A

Spontaneous event/injury → rupture of blood vessel in subarachnoid space → release of blood into CSF →** rapid increase in intracranial pressure**

245
Q

Causes of subarachnoid haemorrhage

A
  • Traumatic → head injury
  • Spontaneous → arterial origin (more common)
    • Arteriovenous blood vessel malformations
    • Rupture of saccular ‘berry’ aneurysms (e.g. anterior half of circle of Willis)
246
Q

What is a symptom of raaised intracranial pressure?

A

THUNDERCLAP HEADACHE
- ‘Worst ever’ headache
- May be only symptom
N+V

247
Q

What is a major complication of a subarachnoid haemorrhage?

A

ASPEPTIC MENINGITIS
- Bleeding into subarachnoid space filled with CSF → blood degradation → irritation of meninges → development of aseptic meningitis
- Neck pain + stiffness
- Photophobia
- Brudzinksi’s (force neck flexion → spontaneous knee, hip flexion)

248
Q

If a patient who has thought to have a subarachnoid haemorrhage, is experiencing neck pain + stiffness and photophobia. What might have they developed?

A

Aseptic meningitis
(Meningeal irritation)

249
Q

What cranial nerve may be affected in increased intracranial pressure? How might this present?

A

Increased intracranial pressure → abducens nerve paralysis → eye pointing out → diplopia

250
Q

Complications of a subarachnoid haemorrhage

A
  • Vasospasm → delayed ischaemia
  • Hydrocephalus
    • Clogging of CSF drainage
  • Re-bleeding
  • Sympathetic hyperactivity due to increased intracranial pressure
    • SAH (’sympathetic surge’)
    • Sudden life-threatening increase in blood pressure - due to vasoconstriction
  • Meningitis (irritation from presence of blood)
  • Seizures
251
Q

Ix for subarachnoid haemorrhage

A
  • Head CT (non-contrast)
    • Hydrocephalus (’Mickey Mouse’ ventricular system appearance
  • MRI
    • Visualise arteriovenous malformations (not detected by angiography)
  • Lumbar puncture
    • Increase erythrocytes in all samples
    • CSF centrifugation → yellow coloration (due to erythrocytes breakage)
  • Fundoscopy (optic disc swelling)
252
Q

Tx for subarachnoid haemorrhage

A
  • Antihypertensive therapy
    • Beta-blockers
    • Hydralazine
    • Calcium channel blockers
    • ACEi
  • Intracranial pressure treatment
    • Osmotic or loop diuretics
  • Prior all procedures: IV midazolam (initial treatment)
  • Vasoconstriction treatment
    • Calcium channel blocker
  • Seizure treatment (phenytoin, phenobarbital)
    Keep blood pressure <140 mmHg to avoid re-bleeding
253
Q

Where does a subdural haemorrhage occur?

A

Intracranial bleeding with blood accumulation between dura mater + arachnoid membrane

254
Q

Causes of a subdural haemorrhage

A
  • Head trauma (most common)
  • Acceleration-deceleration (coup-contrecoup injury)
  • Shaken baby syndrome
  • Spontaneous (vascular malformations)
255
Q

Risk factors for a subdural haemorrhage

A
  • Brain atrophy elderly → bridging veins stretch
  • Infants, alcohol abusers → thinner wall of bridging veins
  • Epilepsy, anticoagulant drugs, thrombocytopenia
256
Q

Sign and symptoms of a subdural haemorrhage

A
  • **Loss of consciousness **after trauma/in ensuing days due to haematoma expansion
  • Acute subdural haematoma
    • Sudden, severe headache, with nausea + vomiting
    • Unequal pupils
    • Difficulties in speech + swallowing
    • Palsies of cranial nerves
  • Chronic (present 14 days after injury)
    • Impaired cognitive skills
    • Altered consciousness
    • Headaches
    • Contralateral/ipsilateral hemiparesis (depends on haematoma location)
    • Optic disc swelling
257
Q

How does a subdural haemorrhage appear on a head CT?

A

Cresent shape

258
Q

Management of a subdural haemorrhage

A

Medications:******

  • Diuretics (decrease intracranial pressure)
  • Vitamin K (anticoagulation reversal)
    • Lower risk of haematoma enlargement

****Surgery:****

  • If clot thickness > 10mm, midline shift > 5mm, intracranial pressure > 20 mmHg
  • Burr Hole
  • Decompressive craniectomy
  • Craniotomy
  • Blood vessel ligation
259
Q

What is used for anticoagulation reversal to lower the risk of haematoma enlargement?

A

Vitamin K

260
Q

What can used to decrease intracranial pressure?

A

Loop diuretics

261
Q

What is an extradural (epidural) haemorrhage?

A

Nervous tissue compression - due to accumulation of blood in the epidural space

Types: Intracranial + spinal

262
Q

Causes of an epidural haemorrhage

A
  • Neurosurgical procedures complication
  • Trauma

Intracranial epidural haematoma
- Head trauma → pterion skull fracture (most common)
- Blood vessel malformations

Spinal epidural haematoma
- Trauma (e.g. lumbar puncture/epidural anaesthesia)

263
Q

How does an epidural haemorrhage initially present?

A

Initial state of consciousness
* Lucid state
* Delayed neurological deterioration - consequence of enlarging haematoma compression

264
Q

What are the signs of increased intracranial pressure?

A
  • Headache
  • Nausea + vomiting
  • Cushing reflex (↑blood pressure, ↓heart rate, irregular breathing)
  • Focal signs
    • Weakness of extremities on opposite side
    • Dilated pupil on injured side - due to compression of CN III
265
Q

A patient presents with a broken skull with a haematoma + altered conscioussness. Possible diagnosis?

A

Intracranial epidural haematoma

266
Q

A patient presents with radicular back pain (resembles pain from herniated discus), sensory defects and urinary + faecal incontinence. What is a possible diagnosis?

A

Spinal epidural haematoma

267
Q

How does an epidural haematoma present on a NCCT?

A

Biconvex haematoma
(+skull fracture)

268
Q

Treatment of an epidural haemorrhage

A

Medications:
- Mannitol, other osmotic diuretics
- ↑urine excretion, ↓intracranial pressure
- Anticoagulation reversal

Surgery:
- Craniotomy (evacuation of blood mass)
- Laminectomy (↓blood in spinal epidural haematoma)

269
Q

What is meningitis?

A

Inflammation of the meninges surrounding the brain + spinal cord

270
Q

Non-infective causes of meningitis

A
  • Paraneoplastic
  • Drug side effects
  • Autoimmune (e.g. vasculitis, SLE)
271
Q

Mnemonic for bacterial causes for meningitis

A

Explaing Big Hot Neck Stiffness
- E. coli, Group B streptococcus (infants)
- Haemophilus influenzae (older infants, kids)
- Neisseria meningitidis (young adults)
- Streptococcus pneumoniae (elderly)

272
Q

Name two diplococci bacteria that cause meningitis

A
  • Strep pneumoniae – most common in adults
    • Gram POSITIVE diplococci
  • Neisseria meningitidis
    • Gram NEGATIVE diplococci
273
Q

Name a parasitic cause of meningitis

A

P. Falciparum

274
Q

What are 4 risk factors for meningitis

A

SPIT:
* Students
* Pregnancy
* Immunocompromised
* Travel

275
Q

What are the three major presentations for meningitis?

A
  • Fever
  • Headache
  • Neck stiffness (‘meningism’)
276
Q

What are 2 clinical signs (tests) for meningitis?

A
  • Kernig’s sign
  • Brudzinksi’s sign
277
Q

What are some signs of meningitis?

A
  • Non-blanching/blanching purpuric rash
    • Glass test
    • Non-blanching: meningococcal septicaemia - bacterial meningitis
  • Photophobia/phonophobia
  • Papilloedema (swelling of optic disc on fundoscopy)
    • Usually bilateral
278
Q

What is the immediate/first line treatment for meningitis?

A

IM benzylpenicillin
(before investigations)

279
Q

First line treatment/investigations for meningitis

A
  • IM bensylpenicillin
  • Assess GCS
  • Blood culture (BEFORE antibiotics)
  • Broad-spectrum antibiotics
    • First line: Cefotaxime or ceftriaxone
    • Immunocompromised: + amoxicillin
    • Recent travel: + vancomycin
  • Steroids: IV dexamethasone
  • LUMBAR PUNCTURE (diagnostic)
    • Microscopy
    • Gram stain
    • Culture
    • Viral PCR
    • Consider Acid Fact Bacilli (TB)
  • CT head
280
Q

Contraindications for a lumbar in meningitis

A
  • Abnormal clotting
  • Petechial/purpura
    • Because suggests bloodborne virus so could introduce bacteria into CSF
  • Raised intracranial pressure (papilloedema)
281
Q

DDx for meningitis

A
  • ‘Worst headache ever’ → subarachnoid haemorrhage (especially if trauma, ‘thunderclap onset’)
  • Migraine
  • Encephalitis
  • Flu and other illnesses
  • Sinusitis
  • Brain abscess
  • Malaria
282
Q

Name 3 major complications of meningitis

A
  • Cerebral oedema
  • Cerebral abscess
  • Venous sinus thrombosis
283
Q

What is the protein level in CSF in meningitis?

A

High protein content

284
Q

What is encephalitis?

A
  • Encephalitis = inflammation of brain parenchyma
  • Associated with neurological dysfunction
    • Altered state of consciousness
    • Seizures
    • Personality changes
    • Cranial nerve palasies
    • Speech problems
    • Motor + sesnory deficits
285
Q

What is the most common cause of encephalitis?

A
  • Viral - HERPES SIMPLEX (most common)
  • Varicella zoster (chicken pox)
286
Q

Which lobes are primarily affected in encephalitis?

A
  • Frontal + temporal lobes
    Results in:
  • Decreased consciousness
  • Confusion
  • Focal signs
287
Q

Pathology of encephalitis

A
  • Peripheral nerve conduits to brain parenchyma (for virus - herpes simplex virus)
  • Haematogenous spread (transer of infections from distant sites)
288
Q

Presentation of encephalitis

A
  • Preceding ‘flu-like’ illness

Then (triad): ACUTE ONSET FEBRILE ILLNESS + ALTERED MENTAL STATUS
* Altered GCS (confusion, drowsiness, coma)
- Seizure, memory loss
* Fever
* Headache

289
Q

What neurological condition could lead to encephalitis?

A

Meningitis
(Patient may meningism presentation aswell as encephalitis)

290
Q

Ix for encephalitis

A
  • Lumbar puncture
    • CSF for viral PCR, serology
    • Raised lymphocytes
  • CT head (if lumbar puncture is contraindicated)
  • MRI after lumbar puncture
    • Show swelling/ inflammation ± midline shifting due to raised ICP
  • Blood cultures
  • Throat swab
  • HIV testing
    • Acute phase viraemia can cause encephalitis
  • EEG
291
Q

What is the treatment for encephalitis?

A
  • Aciclovir IV
  • Supportive care
  • Carbamazepine (seizures)
  • IM benzylpenicillin (meningitis)
292
Q

Complications of encephalitis

A
  • Raised intracranial pressure
  • Seizures
  • Coma
293
Q

What should be administered as soon as you suspect encephalitis?

A

Aciclovir

294
Q

What is motor neuron disease?

A
  • Umbrella term
  • Prossive → ultimately fatal
  • **Motor neurons stop functioning **
295
Q

What happens to the motot + sesnory neurons in motor neuron disease?

A
  • Motor neurons = stop functionng
  • Sensory neurons = not affacted
    • Patients should have no sensory symptoms
296
Q

What is amytrophic lateral sclerosis (ALS)?

A
  • = motor neuron disease
  • Loss of motor neurons in motor cortex + anterior horn
  • UMN + LMN signs = most common
297
Q

How does amytrophic lateral sclerosis (ALS) present?

A
  • Progressive focal wasting
  • Weakness + fasciculation (muscle twitching) spreading to other limbs
  • Cramps
  • Spasticity
  • Brisk reflexes
298
Q

How does primary lateral sclerois present?

A

**UMN signs only **
* Slow progressive tetraparesis
* Pseudobulbar palsy

299
Q

How does progressive muscular atrophy present?

A

LMN signs only
* Weakness + fasciculations in one limb → progressing to adjacement spina segments

300
Q

How does progressive bulbar palsy present>

A

UMN + LMN + Cranial nerve 9,10,11,12 signs
Lower cranial nuclei affected causing:
* Dysarthria (difficultly speaking)
* Dysphagia
* Nasal regurgitation of fluids
* Choking

301
Q

Who is motor neuron disease most likely to present in?

A

Middle aged men

302
Q

Where do upper motor neurons start and travel through?

A
  • UMN = in the motor cortex (in pre-frontal gyrus)
  • Axons travel through hemispheres into spinal cord - via corticospinal tract
303
Q

Where do lower motor neurons start?

A

LMNs = sit in motor nuclei in various parts in the brain stem + all way down the spinal cord in cord in columns in the ventral horn of the spinal grey matter

304
Q

Read: Organistaion of movement

A
  • Idea of movement – association areas of cortex
  • Activation of upper motor neurons in the pre-central gyrus
  • Impulses travel to lower motor neurons and their motor units via the corticospinal (pyramidal) tracts
  • Modulating activity of the cerebellum and basal ganglia
    • Hence why individuals with cerebellar and basal ganglia disorders can’t control movements properly
  • Further modification of movement depending on sensory feedback
305
Q

Read: Regulation of muscle tone

A
  • Stretch receptors in muscle (muscle spindles) innervated by gamma motor neurons
  • Muscle stretched 🡪 afferent impulses from muscle spindles which 🡪 reflex partial contraction of muscle
  • Disease states e.g. spasticity and extrapyramidal rigidity alter muscle tone by altering the sensitivity of this reflex
306
Q

What gene is implicated in motor neuron disease pathology?

A

SOD-1 gene mutation
Suggests** oxidative stress + free radicals** are implicated in the destruction

307
Q

Name 3 Rx for motor neuron disease

A
  • Smoking
  • Exposure to heavy metals
  • Certain pesticides
308
Q

Pathology of motor neuron disease

A
  • Degenerative condition affecting motor neurons – mainly the anterior horn cells
  • There is relentless and unexplained destruction of UMN and anterior horn cells in the brain and spinal cord
  • Causes both UMN and LMN dysfunction
  • UMN and LMN affected but no sensory or sphincter loss – distinguishes from MS
  • Never affects eye movements – distinguishable from myasthenia gravis
309
Q

What signs/symptoms distinguish motor neuron disease from MS and myasthenia gravis?

A

MS vs MND: MND = UMN + LMN affected but no sensory or sphincter loss
Mysthenia gravis vs MND: MND = never affected the eyes

310
Q

Read: Diseases that affect final common pathways

A
  • Motor neurons of the brainstem or spinal cord → Motor neuron disease, spinal cord/brainstem compression
  • Spinal rooys → tumours
  • Peripheral nerve → axonal degeneration or demyelinating
  • NMJ → Myasthenia Gravis
311
Q

Onset of motor neuron disease

A

Insidious + progressive onset

312
Q

Name a sign of motor neuron disease

A

Slurred speech (dysarthria)

313
Q

Name some general motor neuron disease symptoms

A
  • Insidious, progressive weakness of the muscles throughout the body
    • Limbs
    • Trunk
    • Face
    • Speech
  • Weakness = often first noticed in the upper limbs
  • May have increased fatigue when exercising
  • Complain of clumsiness (dropping things, tripping over)
  • Headache in morning (nocturnal hypercapnia)
314
Q

What are some symptoms of lower motor neuron disease?

A

EVERYTHING GOES DOWN!
- Reduced muscle tone (flaccid)
- Fasciculations (twitches in the muscles)
- Reduced reflexes (hyporeflexia)
- Muscle wasting
- Bulbar → speech + swallowing muscles
- Upper limb → hand muscles
- Lower limb
- Bilateral foot drop (from wasting of tibialis anterior muscle) → prominent tibial bones
- Respiratory → weakness of breathing muscles
- Diaphragm = higher up
- Most patients = die from respiratory issues

315
Q

What are some symptoms of upper motor neuron disease?

A

EVERYTHING GOES UP
- Increased tone (spasticity)
- Hyperreflexia → Brisk reflexes
- Upgoing/extensor plantar responses (positive Babinski sign)
- When you stroke sole of foot, normally big toe should go down
- Goes up in UMN lesions
- Characteristic pattern of limb muscle weakness (pyramidal pattern)
- Upper limb extensor muscles = weaker than flexors
- Lower limb flexor muscles = weaker than extensors
- Finer, more skilful movements most severely impaired
- Pyramidal drift
- Hold hands out → one arm will ‘drift away’

316
Q

What does a positive Babinski sign indicate?

A

(Upgoing/extensor plantar responses)
- When you stroke sole of foot, normally big toe should go down
- Goes up in UMN lesions

317
Q

What is pyramidal shft? When is it found?

A

Hold hands out → one arm will ‘drift away’
Found in upper motor neuron disease

318
Q

What is the diagnosis criteria for motor neuron disease?

A

Diagnosis = based on clinical presentation + excluding other conditions that can cause motor neurone symptoms
* Definite = LMN + UMN signs in 3 regions

319
Q

What Ix should you request for UMN lesions?

A
  • MRI spine + brain
  • Blood tests for metabolic disorders
  • Lumbar puncture: CSF examinations (e.g. oligoclonal bands (MS))
320
Q

What Ix should you request for LMN lesions?

A
  • MRI brain + spine
  • Neurophysiology nerve conduction studies/electromyography
  • Blood tests
    • Raised creatinine kinase (due to muscle destruction)
    • Peripheral neuropathy screen
    • Auto-antibodies
  • Lumbar puncture (exclude inflammatory causes)
321
Q

Read: Diagnostic tips for motor neuron disease

A
  • Non sensory loss → rule out MS or myelopathy
  • No disturbances in eye movements → rule out myasthenia gravis or multiple sclerosis (MS)
  • No spincter disturbances → rules out MS
322
Q

Differential diagnoses for motor neuron disease

A
  • Multiple sclerosis (MS)
    • UMN and LMN affected but no sensory or sphincter loss – distinguishes from MS
  • Myasthenia gravis
    • Never affects eye movements – distinguishable from myasthenia gravis
  • **Cervical spine lesion****
    • May present with UMN + LMN signs in arms + legs
  • Idiopathic multifocal motor neuropathy
    • Presents with weakness → predominantly in hands
    • Profuse fasciculation
323
Q

Differential diagnoses for motor neuron disease

A
  • Multiple sclerosis (MS)
    • UMN and LMN affected but no sensory or sphincter loss – distinguishes from MS
  • Myasthenia gravis
    • Never affects eye movements – distinguishable from myasthenia gravis
  • Cervical spine lesion
    • May present with UMN + LMN signs in arms + legs
  • Idiopathic multifocal motor neuropathy
    • Presents with weakness → predominantly in hands
    • Profuse fasciculation
324
Q

Is there a cure for motor neuron disease?

A

No

325
Q

What is the first line drug in motor neuron disease?

A

Riluzole
* (sodium channel blocker → inhibits glutamate release)
* Can slow disease progression → extend survival by a few months in ALS

326
Q

Give two examples of symptom management for motor neuron disease

A
  • Dysphagia → NG/PEG tube
  • Drooling (due to bulbar palsy) → oral amitryptyline
  • Spasticity → baclofen
  • Joint pain → analgesia
  • Non-inasive ventilation (NIV)
    • Supports breathing at night (for nocturnal hypercapnia)
327
Q

Complications of motor neuron disease

A
  • Respiratory failure or pneumonia
    • Patients usually die of this
  • Aspiration pneumonia
328
Q

What is the median survival for ALS?

A

3-5 years

329
Q

Name a cause of an upper motor lesion

A
  • Stroke
  • Infection
  • Tumour
    (Any injury to the brainstem or spinal cord = can cause upper motor neuron lesions)
  • Specifically the WHITE MATTER of the spinal cord (where the upper motor neurons are travelling through)
330
Q

Where can damage occur to cause a lower motor neuron lesion?

A

Any damage to the spinal cord (grey matter) or axons leaving the spinal cord to the skeletal muscle

  • Specifically to the VENTRAL GREY MATTER of the spinal cord (the anterior horn of the spinal cord)
    -** Anterior horn of the spinal cord** = where the UMNs and LMNs synapse (where the LMNs = start)
331
Q

A patient presents with muscle weakness, but no atrophy. Reflexes are increased w/ a positive Babinski sign. Patient does no experience fasciculations. When holding their hands out, one arm will drift away. Possible diagnosis?

A

Upper motor lesion

Pyramidal drift = Hold hands out → one arm will ‘drift away’

332
Q

A patient presents with muscle weakness and atrophy. They have diminshed/absent deep tendon reflex. They also have flaccid paralyis w/ no plantar response. They alos experience fasiculations. Possible diagnosis?

A

Lower motor neuron lesion

333
Q

CN I (Olfactory) Palsy Sx

A

Anosmia - can’t smell

334
Q

CN II (Optic nerve) paslsy Sx

A

Visual defect - depends on location

335
Q

CN III (oculomotor) palsy Sx

A
  • Ptosis = drooping of eyelids
  • Fixed pupil dilation
  • Eye down + out
336
Q

Causes of a CNIII palsy

A
  • Raised ICP
  • Diabetes
  • Hypertension
  • Giant cell arteritis
337
Q

CN IV (trochlear) palsy Sx

A

Diplopia (double vision) on looking down (e.g. walking down the stairs)

338
Q

CN V (trigeminal) palsy Sx

A
  • Jaw deviates to the side of the lesion
  • Loss of corneal reflex
    • Involuntary blinking of the eyelids elicited by stimulation of the cornea
339
Q

CN VI (abducens) palsy Sx

A

Eyes abducted

340
Q

Causes of CN VI (abducen’s) palsy?

A
  • MS
  • Wernicke’s encephalopathy
  • Pontine stroke (fixed small pupils)
341
Q

CN III, IV, VI (3,4,6) Palsy

A

Non-functioning eye
Causes:
* Stroke
* Tumours
* Wernicke’s encephalopathy

342
Q

CN VII (facial) palsy Sx

A

Facial droop + weakness

343
Q

Name a major cause of CN VII (facial) nerve palsy and the treatment

A

Bell’s palsy
(dribbling at side of mouth)

Management = steroids

344
Q

Difference in presentation between Bell’s palsy and stroke

A
  • Bell’s palsy → forehead + lip droop
  • Stroke → Lip droop
345
Q

CN VIII (vestibulocochlear) palsy Sx

A
  • Hearing impairment
  • Vertigo + lack of balance
346
Q

CN IX (glossopharyngeal) and CN X (vagus) palsy Sx

A
  • Gag reflex issue
  • Swallowing issues → uvula = deviates from the side of the lesion
  • Vocal issues
347
Q

CN XI (accessory) palsy

A

Cannot shrug shoulder or shake head

348
Q

CN XII (hypoglossal) palsy Sx

A

Tongue deviates towards side of lesion

349
Q

What is Brown-Sequard syndrome?

A

Hemisection of the spinal cord

350
Q

Name some causes of spinal cord compression

A
  • Trauma
  • Spinal cord tumours
  • A prolapsed intervertebral disc (herniation)
  • Epidural or subdural haematoma
  • Inflammatory disease (esp. rheumatoid arthritis)
  • Spinal infection
  • Cervical spondylitic myelopathy
  • Spinal manipulation
351
Q

Where is the most common site for a prolapsed intervertebral disc (herniation)

A

L4-L5 and L5-S1
(Large disc herniations can cause cauda quina syndrome)

352
Q

What are the sensory and motor symptoms of spinal cord compression

A

Sensory symptoms = sensory loss + paraesthesia
* Light touch + proprioception + joint position sense = reduced

Motor symptoms = fatigue + gait disturbance

353
Q

What is the presntations of:
* Cervical spine
* Thoracic spine
* Lumbar spine

A
  • Cervical spine lesion → quadriplegia + artifical ventilation = required
    • Injury above level C3,C4, C5 (the segmental level of the phrenic nerve) → causes paralysis of the diaphragm → artificial ventilation is required
  • Thoracic spine lesion → paraplegia
  • Lumbar spine lesions → can affect L4, L5 and sacral nerve roots
354
Q

What is the investigation for spinal cord compression?

A

MRI spine

355
Q

What is metastatic spinal cord compression?

A

When a metastatic lesion = compresses the spinal cord (before the end of the spinal cord and the start of the cauda equina)
* It is an oncological emergency

356
Q

What is the difference between metastatic spinal cord compression and cauda equina syndrome?

A
  • Cauda equina syndrome = presents with LMN signs (reduced muscle tone + reduced reflexes)
  • Metastatic spinal cord compression = UMN signs seen (increased tone, brisk reflexes, upping plantar responses)
    • Spinal cord = being compressed higher up
357
Q

Where is compression in sciatica?

A

L5/S1 root compression

358
Q

What is radicular pain?

A

Radiating shooting pain

359
Q

Name a spinal and non-spinal cause of sciatica

A
  • Spinal: Spinal disc herniation
  • Non-spinal: Pregnancy
360
Q

How does sciatica present?

A

Unilateral sudden shooting pain radiating from lumbar spine down leg (side , back) to foot
* Pain: Lower back, buttock, hip and foot
* Numbness, muscle weakness, burning sensation

361
Q

What Ix/tests do you perform for sciatica?

A
  • MRI/x-ray
  • Straight leg raising test
  • Crossed straight leg raising test (higher specificity)
362
Q

First and second line management for sciatica

A
  • Fist line: Analgesia (NSAIDs)
  • Secon line: Surgical decompression, spinal disc repair (severe symptoms)
363
Q

What is cauda equina syndrome?

A
  • Cauda equina = formed by the nerve roots distal to the termination of the spinal cord at L2/L3
  • Cauda equina syndrome = caused by compression of the lumbosacral nerve roots of the cauda equina
  • CES is a neurosurgical emergency, and delays in diagnosis and treatment may lead to permanent disability.
364
Q

Caues of cauda equina syndrome

A
  • Lumbar disc herniation at L4/L5 and L5/S1
  • Tumours
  • Spondylolisthesis(anterior displacement of a vertebra out of line with the one below)
  • Abscess
  • Trauma
365
Q

What is the cauda equina?

A
  • Cauda equina = collection of roots - that travel through the spinal canal AFTER the spinal cord terminate around L2/L3
  • The nerve roots = exit either side of the spinal column at their vertebral level
    • (L3, L4, L5, S1, S2, S3, S4, S5 and Co)
366
Q

What does the cauda equina supply?

A
  • Sensation → lower limbs + perineum + bladder + rectum
  • Motor innervation → lower limbs + anal and urethral sphincters
  • Parasympathetic innervation → bladder + rectum
367
Q

What os the treatment of metastatic spinal cord compression?

A
  • High dose dexamethasone (to reduce swelling in the tumour and relieve compression)
  • Analgesia
  • Surgery
  • Radiotherapy
  • Chemotherapy
368
Q

What is the menomic for cauda equina syndrome presentation?

A

SPINE
* S- Saddle anaesthesia
* P - Pain
* I - Incontinence
* N - Numbness
* E - Emergency

BLADDER DYSFUNCTION = essential component of CES

369
Q

Other Sx of cauda equina syndrome

A

Signs:
* Fasciculations
* Urinary retenion

Symptoms:
* **Saddle anaesthesia **
* Less bladder + bowel control
* Erectile dysfunction
* Lumbosacral pain
* Leg weakness - flaccid + areflexic
* Paraplegia

370
Q

What are the first and gold-standard investigations for cauda equina syndrome?

A

First line:
* Digital rectum examination
* Examination (knee flexion, straight leg raising)

Gold standard:
* MRI lumbar spine (without contrast)

371
Q

Treatment for cauda equina syndrome

A
  • Immediate hospital admission → MRI spine
  • Neurosurgical input → lumbar decompression surgery of the spinal cord
372
Q

Complications of cauda equina syndrome

A
  • Bladder dysfunction
  • Bowel dysfunction
  • Sexual dysfunction
  • Back and/or leg pain
  • Sensory pain
  • Leg weakness
373
Q

Define syncope

A

Event of temporarily losing consciousness - due to a disruption of blood flow to the brain → often leading to a fall

374
Q

What are the 3 major criteria for syncope?

A
  • Loss of consciousness
  • Loss of consciousness = must be TRANSIENT (self-limiting)
  • Caused by GLOBAL CEREBRAL HYPOFUSION (almost always means BP)
375
Q

Name some causes of primary syncope (simple fainting)

A
  • Dehydration
  • Missed meals
  • Extended standing in a warm environment, such as a school assembly
  • A** vasovagal response to a stimuli**, such as sudden surprise, pain or the sight of blood
376
Q

Pathophysiology of syncope

A
  • Strong stimulus (emotional event, painful sensation, change in temp) → stimulates vagus nerve → stimulates parasympathetic nervous system
  • Blood vessels delivering blood to the brain = relax → BP in the cerebral = drops → hypoperfusion of brain tissue → patient = loses consciousness and ‘faint’
377
Q

Ix for syncope

A
  • ECG (arrhythmia + long QT syndrome)
  • Bloods (FBC: Anaemia; Electrolytes: Arrhythmias + seizure; Blood glucoese)
  • Neurological examination
  • Lying and standing blood pressure
  • Tilt-table testing
378
Q

What is tilt table testing used to diffrentiate between?

A

Vasovagal syncope + Postural (orthostatic) hypotension syncope

379
Q

What is Lambert-Eaton Myasthenic Syndrome?

A

Rare autoimmune disorder of the neuromuscular junction
Pesents like myasthenia gravis - but less severe +** weakness improves with exercise**

380
Q

What primarily causes Lamber-Eaton Myasthenic Syndrome?

A

Small Cell Lung Cancer (Paraneoplastic)

381
Q

Pathology of Lambert-Eaton Myasthenia Syndrome

A

Antibodies produced that damage the voltage-gated calcium channels in the presynaptic terminals of the NMJ (not enough ACh release)

382
Q

Presentation of Lambert-Eaton Myasthenia Syndrome

A

- Symptoms develop very slowly
- Proximal muscle weakness → proximal leg muscle weakness

  • Eyes
    • Diplopia
    • Ptosis
  • Oropharyngeal muscles
    • Slurred speech
    • Dysphagia (swallowing problems)
  • Autonomic dysfunction
    • Dry mouth
    • Dizziness
    • Impotence
    • Blurred vision
  • Reduced tendon reflexes
383
Q

Ix for Lambert-Eaton Myasthenic Syndrome

A
  • Nerve conduction studies
  • Chest CT scan (underlying malignancy)
  • Anti-P/Q voltage-gated calcium channel serology (positive)
384
Q

Treatment for Lambert-Eaton Myasthenia Syndrome

A
  • Treat uderlying cause
  • Amifampridine orally
  • Immunosuppressants (prednisolone or azathioprine)
385
Q

What is a meningioma?

A

Benign brain tumour

386
Q

What is a glioblastoma?

A

Highly malignant brain tumour

387
Q

How do brain tumours present?

A
  • Often asymptomatic
  • Focal neurolofical symptoms
  • Raised intracranial pressure
388
Q

A patient has had an unusual change in personality and behaviour. Where would the location of a brain tumour be?

A

Frontal lobe
(Frontal lobe = responsible for personality + higher-level decision making)

389
Q

What is a key symptom of raised intracranial pressure?

A

Headache:
* Constant
* Nocturnal
* Worse on waking
* Worse on coughing, straining or bending forward
* Vomiting

390
Q

What is a key examination finding for raised intracranial pressure?

A

Papilloedema on fundoscopy

391
Q

Name a couple of causes of raised intracranial pressure

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection

392
Q

Apart from headache, what are some other features of raised ICP?

A
  • Altered mental state
  • Visual field defects
  • Seizures (particularly focal)
  • Unilateral ptosis
  • Third and sixth nerve palsies
  • Papilloedema (on fundoscopy)
393
Q

Name common cancers that metastasise to the brain

A
  • Lung
  • Breast
  • Renal cell carinoma
  • Melanoma
394
Q

What is a glioma?

A

Tumuours of the glial cells in the brain or spinal cord

395
Q

What is the most malignant glioma?

A

Gliobastoma multiforme
(Also most common)

396
Q

What is a meningioma?

A

Tumours growing from the cells of the meninges in the brain + spinal cord
* Usually benign
* Mass effect - can lead to raised intracranial pressure + neurological symptoms

397
Q

What visual defect can pituitary tumours cause if large enough?

A

Bitemporal hemianopia
(Press on the optic chiasm)

398
Q

What brain tyumour is associated with hearing loss, tinnitus and balance problems?

A

Acoustic neuroma (AKA Vestibular Schwannoma)

399
Q

What is the general management of brain tumours

A
  • Palliative care
  • Chemotherapy
  • Radiotherapy
  • Surgery
400
Q

Carpal tunnel syndrome is caused by the compression of which nerve?

A

Median nerve

401
Q

What causes bilateral carpal tunnel syndrome?

A
  • Rheumatoid arthritis
  • Diabetes
  • Acromegaly
  • Hypothyroidism
402
Q

Which finger is not affected in carpal tunnel syndrome?

A

Little finger

403
Q

What are the sensory symptoms of carpal tunnel syndrome?

A
  • Pain
  • Numbness
  • Paraesthesia (pins + needles, tingling)
  • Burning sensation
404
Q

What are the motor symptoms of carpal tunnel syndrome?

A
  • Weakness of thumb movements
  • Weakness of grip strength
  • Difficulty with fine movements
  • Wasting (atrophy of thenar muscles)
405
Q

What does a positive Phalen’s test indicate?

A

Carpal tunnel syndrome
- Position triggers the sensory symptoms of carpel tunnel
- Numbness + paraesthesia in the median nerve distribution

406
Q

What does a positive Tinel’s test indicate?

A

Carpal tunnel syndrome
- Tap the wrist at where the median nerve travels through the carpal tunnel (in the middle - at the point where the wrist meets the hand)
- Position triggers the sensory symptoms of carpel tunnel
- Numbness + paraesthesia in the median nerve distribution
- TOM TIP: Think of tapping a tin can (Tinel’s) to remember the difference between Phalen’s and Tinel’s test.

Think of tapping (Tinel’s) to remember between Phalen’s & Tinel’s test.

407
Q

What are the two clinical examination tests for carpal tunnel syndrome?

A
  • Phalen’s
  • Tinel’s
408
Q

What is the diagnostic test for carpal tunnel syndrome?

A

Nerve conduction studies (electromyography)

409
Q

Managment for carpal tunnel syndrome

A
  • Wrist splints
  • Steroid injections (hydrocortisone or methylprednisolone acetate)
  • Surgical decompression
410
Q

Injury in to the radial nerve results in which condition?

A

Wrist drop
- = Inability to extend the wrist (+ fingers) → due to weakness or paralysis of the POSTERIOR FOREARM MUSCLES

411
Q

Claw hand is a result from what?

A
  • Ulnar nerve palsy
  • Charcot-Marie-Tooth Disease
412
Q

What is a radiculopathy and give an example?

A
  • Radiculopathy = compression of nerve root + LMN
  • Sciatica = lumbar radiculopathy
    (cranial nerves = peripheral - because they have Schwann cells)
413
Q

What is a mononeuropathy and give an example?

A
  • Mononeuropathy = affects 1 nerve
  • Carpal tunnel syndrome (medial nerve) = most common
  • Cranial mononeuropathies (III or VII cranial nerve palsy)
414
Q

What is a polyneuropathy and give an example?

A

Polyneuropathy = multiple/systemic - can be motor, sensory, sensorimotor and autonomic
* Multiple sclerosis
* Guillain-Barre
* Diabetes

415
Q

What are the 6 mechanisms that cause nerve malfunction?

A
  • Demyelination
  • Axonal degeneration
  • Compression
  • Infarction (micro-infarction of the nvasa nervorum)
  • Infiltration
  • Wallerian degeneration
416
Q

What are the causes of peripherpheral neuropathy?

A

DAVID:
* D - Diabetes
* A - Alcohol
* V- Vitamin B12 deficiency
* I - Infective
* Drugs - isoniazid

417
Q

Name two systemic onditions that commonly cause axonal peripheral neuropathy

A
  • Diabetes
  • Vitamin B12 deficiency
418
Q

Name the motor symptoms of peripheral neuropathies

A
  • Muscle cramps
  • Weakness
  • Fasciculations (muscle twitches)
  • Muscular atrophy → excessive atrophy → high arched feet (pes cavus)
419
Q

What anti-neuralgics can you give for peripheral neuropathies?

A

GAP:
* Gabapentin
* Amytriptyline
* Pregabalin

420
Q

Ix for peripheral neuropathies

A
  • Clinical examination
    • Reduced or absent reflexes
    • Sensory deficit
    • Weakness → muscle atrophies
  • Neurological examination (nerve conduction studies/QST)
    • Demyelinating → slow conduction velocities
    • Axonal → reduced amplitudes of the potential
421
Q

What is mononeuritis multiplex?

A

Used to describe a distinctive clinical presentation of progressive motor + sensory deficits in the distribution of specific peripheral nerves

422
Q

How does Brown Sequard syndrome present>

A
  • Contralateral: pain + temperature loss
  • Ipsilateral: hemiparesis/hemiplegia + proprioception/vibration sense loss
423
Q

Management ofr Brown-Sequard Syndrome

A
  • Supportive - physical + occupational therapy
  • Steroids - reduce swelling + inflammation
424
Q

What is Charcot-Marie-Tooth disease?

A
  • a group of hereditary peripheral neuropathies with different genetic abnormalities.
    • Usually autosomal dominant pattern
425
Q

Presentation of Charcot-Marie-Tooth syndrome?

A
  • Walking difficulties
  • Pes cavus (high foot arches)
  • Steppage gait
  • Diffuse deep tendon hyporeflexia or areflexia
  • Reduced muscle strength
  • Reduced sensation
426
Q

What is Duchenne Muscular Dystrophy?

A
  • Muscular dystrophy = umbrella term for genetic conditions - that cause gradual weakening + wasting of muscles
  • Duchenne muscular dystrophy (DMD) = caused by **********defective dystrophin gene********** on the ****x-chromosome****
    • Caused by non-sense/frameshift mutation
    • ********DMD = CONGENITAL MYOPATHY********
    • DMD → Doesn’t Make Dystrophin
427
Q

Management of DMD

A
  • Oral steroids → slow progression of muscle weakness (prednisolone)
  • Creatinine supplementation → improve muscle strength slightly
  • Physiotherapy + exercise + psychological support

Kyla's Phase 2a Flashcards (10 decks)

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