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Conditions + definitions > Neuro conditions 1 > Flashcards

Neuro conditions 1 Flashcards

1
Q

What are the causes of bloackout?

A 
Syncopy
	First seizure
	Hypoxic seizure
	Concussive seizure
	Cardiac arrhythmia
	Non-epileptic attack
		(narcolepsy, movement disorder, migraine
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2
Q

What are the important considerations in a blackout?

A

What were they doing at the time?
What, if any, warning feelings did they get? - aura
What were they doing the night before?
Have they had anything similar in the past?
How did they feel afterwards?
Any injury, tongue biting or incontinence?
Also get witnesses during + before attack

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3
Q

What is syncope?

A 
Vasovagal syncope is the most common cause of fainting
Prodrome:
Light-headed, nausea
Hot, sweating
Tinnitus
Tunnel vision
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4
Q

What are the triggers for vasovagal syncope?

A 
Prolonged standing
Standing up quickly
Trauma
Venepuncture
Watching/experiencing medical procedures
Micturition
Coughing
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5
Q

What are the differences between syncope and seizure?

A

Seizure is a loss of control that can happen in any posture with sudden onset
Often associated with incontinence pallor and injury
Syncope is a loss of consciousness that happens in an upright posture with gradual onset
>Precipitants are common with rapid recovery

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6
Q

What are hypoxic seizures?

A

When kept upright in a faint
Can occur in aircraft, dentist, helped to feet etc
May have succession of collapses
Seizure-like activity may occur

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7
Q

What are non-epileptic attacks?

A 
Commoner in women than men
Can be frequent
May look bizarre
Can be prolonged
May have a history of other medically unexplained symptoms
May have history of abuse
May superficially resemble a generalised tonic-clonic seizure
May resemble a “swoon”
May involve bizarre movements
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8
Q

How do you investigate first seizure?

A

Blood sugar
ECG
Consideration of alcohol and drugs
CT head (see criteria)

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9
Q

What is the advice for driving after seizure?

A

Give safety information
Inform employer
Driving regs - After 6 months if normal investigations, if abnormal/alcohol related 12 months (for both, no recurrent fits)

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10
Q

What features suggest epilepsy?

A

History of myoclonic jerks, especially first thing in morning, absences or feeling strange with flickering lights
– in keeping with a primary generalised epilepsy
History of “deja vu”, rising sensation from abdomen, episodes where look blank with lip-smacking, fiddling with clothes – suggest a focal onset epilepsy

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11
Q

What is epilepsy?

A

Condition in which seizures recur, usually spontaneously

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12
Q

What is a seizure?

A

Seizure - intermittent disturbance of consciousness, behaviour, emotion, motor function or sensation

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13
Q

What are focal seizures?

A

Characterised via aura, motor features, autonomic features + degree of awareness/responsiveness
May involve generalised convulsive siezure

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14
Q

How do you investigate seizures?

A

EEG for primary generalised epilepsies including hyperventilation and photic stimulation: sometimes sleep deprivation
MRI for patients under age 50 with possible focal onset seizures: CT usually adequate to exclude serious causes over this age
Video-telemetry if uncertainty about diagnosis

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15
Q

What are the features of a primary generalised seizure?

A 
No warning
Often below 25
May have history of absences + myoclonic jerks 
Generalised abnormality on EEG
May have family history
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16
Q

What are the features of a focal/partial seizure?

A 
May get aura
Any age - cause can be any abnormality
Simple partial + complex partial can become secondarily generalised
Focal abnormality on EEG
MRI may show cause
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17
Q

What are the first line treatments for primary generalised epilepsy?

A

Sodium Valproate, Lamotrigine, Levetiracetam

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18
Q

What are the first line treatments for partial or secondary generalised seizures?

A

Lamotrigine or Carbamazepine

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19
Q

What is the first line treatment for absence seizures?

A

Ethosuximide

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20
Q

What are the side effects of sodium valproate?

A 
tremor, 
weight gain, 
ataxia, 
nausea, 
drowsiness, 
transient hair loss, 
pancreatitis, 
hepatitis
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21
Q

What are the side effects of carbamezepine?

A 
ataxia, 
drowsiness, 
nystagmus, 
blurred vision, 
low serum sodium levels, 
skin rash.
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22
Q

What is status epilepticus?

A

Prolonged or recurrent tonic-clonic seizures persisting for 30 minutes + with no recovery period between seizures
Usually in patients with no previous history of epilepsy
Mortality 5-10%

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23
Q

How do you treat status epilepticus?

A

Midazolam:
Lorazepam:
Diazepam

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24
Q

What are the symptoms of muscle disorders?

A 
Weakness of skeletal muscle
	Short of breathe (respiratory muscles)
	Cardiomyopathy 
	Poor suck/ feeding/FTT(failure to thrive)/floppy
	Cramp, pain (no ATP)
	Myoglobinuria (black urine)
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25
Q

What are the signs of muscle disorders?

A

Wasting/ hypertrophy
Normal or reduced tone and reflexes
Motor weakness…NOT sensory

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26
Q

What are the investigations into muscle diseases?

A

History + exam (history important)
CK (creatin kinase)
Muscle biopsies (less +less)
Genetic testing

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27
Q

What are the types of muscle diseases?

A 
Muscular dystrophies
	Channelopathies (problem with channels)
	Metabolic muscle disease
	Inflammatory muscle disease
	Congenital myopathies
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28
Q

What are muscular dystrophies?

A

Mostly due to one defective gene

Cause structural problems in muscles

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29
Q

What are channelopathies?

A

Disorders of Ca, Na and Cl channels

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30
Q

What are the metabolic muscle diseases?

A

Disorders of carbohydrate metabolism
First 10 mins difficult, if overcome have stores
Disorders of lipid metabolism - unable to last past 10 minutes
Mitochondrial myopathies/ cytopathies

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31
Q

What is inflammatory muscle disease?

A 
Polymyositis
Dermatomyositis
>Distinctive rash - heliotrophic
>Red over elbows, purple on face
Acute or subacute
Painful weak muscles
Any age
Other symptoms may be involved (arthritis? Interstitial pneumonia both possible)
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32
Q

What is myasthenia gravis?

A 
Fatiguable weakness:
Limbs
Eyelids (ptosis)
Muscles of mastication (chewing)
Talking
SOB
diplopia
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33
Q

Why does myasthenia gravis happen?

A

Due to Anti ACHR ab binding to AcH receptor, preventing contraction

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34
Q

how do you investigate suspected myasthenia gravis?

A

AChR ab
Anti MuSK ab
EMG
Tensilon test (unusual these days as dangerous)

CT chest
>Can be associated with malignant thymoma - always CT to check!!
>Can be caused by it in females under 40, although not always

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35
Q

How do you treat myasthenia gravis?

A

Symptomatic - Acetylcholinesterase inhibitor
Immunosuppression
Prednisolone
Steroid saving agent (azathioprine)

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36
Q

What can cause generalised peripheral neuropathy?

A 
Metabolic: DM, alcohol, B12
	Toxic: drugs
	Hereditary
	Infectious: HIV, leprosy
	Malignancy: paraneoplastic
	Inflammatory demyelinating
	Acute = Guillain Barre syndrome
Chronic= CIDP
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37
Q

What are the symptoms of a nerve root being affecteD?

A

Myotomal wasting and weakness
Reflex change
Dermatomal sensory change

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38
Q

What are the symptoms of an individual nerve bein affected?

A

Wasting and weakness of innervated muscle

Specific sensory change

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39
Q

What are the symptoms of generalised peripheral neuropathy?

A

Sensory and motor symptoms starting distally and moving proximally

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40
Q

How do you investigate nerve disorders

A 
Blood tests
	Genetic analysis
	NCS/EMG
	Lumbar puncture (CSF analysis)
	Nerve biopsy (nb sensory nerve)
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41
Q

What is amyotrophic lateral sclerosis?

A

Usually limb onset, later bulbar and respiratory involvement
combination of UMN and LMN signs
> LMN= muscle fasciculations, wasting, weakness
>UMN= increased tone, brisk reflexes
M:F 3:2

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42
Q

What is the prognosis of ALS?

A

3-5 years from symptom onset
2-3 years from diagnosis
50% die within 14 months of diagnosis
Mostly supportive treatment

43
Q

What is myelopathy?

A

Pathology of spinal cord

44
Q

What is myelitis?

A

Inflammation of spinal cord

45
Q

What is radiculopathy?

A

Pathology of nerve root

46
Q

What is radiculitis?

A

Inflammation of nerve root

47
Q

What is myeloradiculopathy?

A

Pathology of spinal cord leading to pathology of nerve root

48
Q

What are upper motor signs?

A

No wasting
↑tone
Spascisity
↑reflexes

Pyramidal pattern of weakness - in arms, flexors stronger than extensors, opposite in klegs

49
Q

What are lower motor neuron signs?

A

↓tone
↓reflexes
weakness

50
Q

What is brown-sequard syndrome?

A

One side loss of motor + touch on one side, temperature on the other

51
Q

What are the signs of B12 deficient myelopathy?

A 
Paraesthesia hands and feet, areflexia
	First UMN sign ↑plantars
	Degeneration of 
		 corticospinal tracts→paraplegia
		Dorsal columns→sensory ataxia
	Painless retention of urine
May be too late to treat
52
Q

What is the effect of B12 deficency on the nervous system?

A 
Myelopathy
		L’hermitte’s
	Peripheral neuropathy
	Brain 
	Eye/optic nerves
	Brainstem
cerebellum
53
Q

What are teh causes of transverse myelitis?

A 
Viral
	Other infections
		Syphilis, measles, Lyme
	Autoimmune
	Malignancies
Post vaccination (chicken pox, rabies)
54
Q

What is demyelinating myelitis?

A

Characterised by pathological lesions of inflammation and demyelination leading to temporary neuronal dysfunction
Affects the white matter of the CNS
One or more lesions anywhere

55
Q

How do you treat demyelinating myelitis?

A

Supportive

Methylpredinsolone

56
Q

What are the clinical features of ischaemia in spinal cord?

A

May have vascular risk factors
Onset may be sudden or over several hours
Pain
>Back pain/radicular
Weakness
>Usually paraparesis rather than quadraparesis given vulnerability of thoracic cord to flow related ischaemia
Numbness and paraesthesia
Urinary symptoms
>Retention followed by bladder and bowel incontinence as spinal shock settles

57
Q

How do you treat ischaemia in spinal cord?

A 
Supportive
Reduce risk of recurrence
>Maintain adequate BP
>Bed rest
>Reverse hypovolaemia/arrhythmia
OT and physiotherapy
Manage vascular risk factors
58
Q

What can cause myelopathy?

A 
Demyelination
Ischaemia
Transverse myelitis
Metabolic/B12 deficnecy
Malignancy
Lyme/AIDS
Inflammation
59
Q

Where does infaction of the spinal cord normally happen?

A

Normally affects only posterior or anterior side due to blood vessel supply
Radicular arteries off aorta/intercostal muscles
>Thoracic + bottom of s[inal cord poor blood supply
>Rare in posterior (dorsal columns spared) - usually anterior spinal artery
Usually mid thoracic

60
Q

What is demyelination?

A

Auto immune process caused by activated T cells across blood brain barrier
Acute inflammation of myelin sheath
Leads to loss of function
>Repair-recovery of function
Post inflammatory gliosis may have functional deficit
>Lesions/plaques show up on MRIs

61
Q

What is the progression of demyelination?

A

Axonal loss shown by black holes in MRI
Axonal loss may be present from disease onset (unkown)
Later seen as cerebral atrophy

62
Q

Who is likely to get demyelination?

A

Females 3:1
More common further away from equator
Genetic link
Younger populace

63
Q

What is the initial presentation of MS?

A

Gradual onset over days
Stabilises in days-weeks
Gradual resolution to complete or partial

64
Q

What is the clinical presentation of an MS relapse?

A

Optic neuritis
Sensory symptoms
Limb weakness
Brainstem Diplopia/Vertigo/Ataxia-
Spinal cord-bilateral symptoms and signs +/- bladder

65
Q

What is optic/retrobulbar neuritis?

A 
Subacute visual loss
Pain on moving eye
Colour vision disturbed
Usually resolves over weeks
Initial  swelling optic disc
Optic atrophy seen later
Relative afferent pupillary defect
66
Q

What other diseases can cause optic neuritis?

A 
Neuromyelitis optica
	Sarcoidosis
	Ischaemic optic neuropathy
	Toxic/ drugs/ B12 deficiency
	Wegeners granulomatosis
	Local compression
	Lebers hereditary optic neuropathy
\+ others
67
Q

What are the symptoms of a brainstem relapse?

A

Cranial nerve involvement
Pons- internuclear ophthalmoplegia
E.g. Vertigo, nystagmus, ataxia
Upper motor neurone changes limbs

68
Q

What are the symptoms of myelitis?

A

Depends if partial or transverse
Check sensory level
Weakness/UMN changes below level
Bladder+ bowel involvement

69
Q

What is MS?

A

Episodes of demyelination diseminated in space + time
May occur within months or years within first relapse
Variable site/severity
Diagnose with clinical (posers criteria) or MRI (macdonald)
For every 10 lesions on MRI (roughly) patient suffers 1 relapse
Scan+ symptoms may not correlate

70
Q

What is the progressive phase of MS?

A 
Accumulation of symptoms and signs
>Fatigue, temperature sensitivity
>Sensory
>Stiffness or spasms
>Balance, slurred speech
>Swallowing
>Bladder & bowel
>Diplopia/ oscillopsia/ visual loss
>Cognitive-dementia/ emotional lability
71
Q

What are the signs of MS on examination?

A 
Depends on where demyelination has occurred and stage of disease:
>Afferent pupillary defect
>Nystagmus or abnormal eye movements
>Cerebellar signs
>Sensory signs
>Weakness
>Spasticity
>Hyperreflexia
>Plantars extensor
72
Q

How do you investigate MS?

A

MRI
Rest depend on clinical picture……
>Lumbar puncture-oligoclonal bands present in CSF but not serum
>Visual/ somatosensory evoked response
>Bloods-exclude other inflammatory conditions
>Chest X Ray

73
Q

What are the differentials to MS?

A 
Depends on symptoms and signs and on whether a first relapse or progressive disease
Includes:
>Acute Disseminated Encephalomyelitis
>Other Auto-immune conditions eg SLE
>Sarcoidosis
>Vasculitis
>Infection eg Lyme disease, HTLV-1
>Adrenoleucodystrophy etc etc
74
Q

What are the types of MS?

A 
Relapsing remitting-85% at outset (RRMS)
	Secondary progressive (SPMS) 
	Primary progressive – 10-15% (PPMS)
	Sensory – 5%
	Malignant
		Describe the disease
	1/4 will need a wheelchair at some point
75
Q

What is the prognosis for relapse remitting MS?

A 
Difficult to predict, however:
Good for 
>Female
>Present with optic neuritis
>Long interval between 1st + 2nd relapse
>Few relapses in first 5 yrs
Bad for
>Male
>Older age
>Multifocal symptoms + signs
>Motor symptoms + signs
76
Q

What is primary progressive MS?

A 
Often presents in 5th and 6th decade
No relapses
Spinal symptoms
Bladder symptoms
Prognosis poor
M:F = 1:1
77
Q

What is devic’s disease?

A 
Optic neuritis
	Myelitis
	Aquaporin-4 antibodies
	Antibody negative in some cases
	Treat with immuno suppression
78
Q

How do you treat MS?

A 
Beta-interferons/ glatiramer acetate
Daily-weekly im/ sc injection
		Teriflunomide
		Dimethyl Fumarate
>Reduce relapse rate ~1/3
>No effect on progression of disability
>Not a cure
79
Q

What are the side effects of first line MS treatments?

A

Flu-like symptoms
Injection site reaction
Abnormalities of blood count and liver function

80
Q

How should you approach an acute MS relapse?

A

Look for underlying infections
Rehab + symptomatic treatment
Steroids - if not infection

81
Q

How should you treat further MS relapses?

A

Vaccination to prevent

Fewer during pregnancy, increased risk in first 3 months after birth

82
Q

What are the types of brain injury?

A

Direct trauma

Indirect trauma

83
Q

What are the symptoms of brain injury?

A 
Headache
	Nauzea
	Vomiting
	Dizziness
	Hemiparesis
	Seizure
	Double vision
	Cranial nerve/s palsy
	Ataxia
	Slurred speech
	Dysarthria
	Unresponsiveness
	Unconciousness
	Irregular breathing
	Unequal pupils
	Respiratory / Cardiac arrest
84
Q

What are indicatiors of a direct trauma?

A

Bruises
Skull fracture
Closed/open injuries
Extradural haemorrhage

85
Q

What are the indicators of an indirect trauma?

A 
No bruises
Subdural haematoma
Traumatic SAH
Contusion
Diffuse aconal injury
86
Q

What are teh examples of close trauma?

A

Haemrrhage (extra/sub dural)
Traumatic SAH
Contusion

87
Q

How do you treat a brain injury?

A

Surgical - skull cap removal to relieve pressure
Conservative
cSF diversion

88
Q

What is pain?

A

Unpleasant sensory + emotional experience primarily associated with tissue damage

89
Q

What is the pathway of pain?

A 
Periphery
>Detection + transmission to spinal cord
Spinal cord
>Processing + transmission t brain (thalamus)
Brain
>Perception, learning, response
Modulation
>Descending tracts
90
Q

What diseases change perception of pain?

A

Allodynia
Hyperalgesia
Spontaneous pain

91
Q

What is spontaneous pain?

A

Spontaneous activity in nerve fibres

92
Q

What is Allodynia?

A

Decreased threshold for response

93
Q

What is Hyperalgesia?

A

Exaggerated response to normal stimuli

94
Q

What is central centralisation?

A

Response of second order neurone in CNS to both noxious + non noxious stimuli
Wind up, classical + long term potentiation components

95
Q

What is wind up?

A

Involves only activated synapses
Homosynaptic activity dependent progressive increase in response of the neurons
Manifests over the course of stimuli & terminates with stimuli

only in neurons taking part in the synapses with primary afferent input.
It is activity dependent; progressively increases the response of the neurons.
terminates with stimulus.

96
Q

What is central sensation?

A

Involves opening up of new synapses (silent nociceptors)
Heterosynaptic activity dependent plasticity
Immediate onset with appropriate stimuli
Outlast the initial stimuli duration
Can be maintained even at low levels of ongoing stimuli

97
Q

What is long term potentiation?

A

Involves mainly the activated synapses
Occurs primarily for
very intense stimuli

98
Q

What is nocioceptive pain?

A

Painful region is typically localised at the site of injury – often described as throbbing, aching or stiffness
Usually time limited and resolves when damaged tissue heals (e.g. bone fractures, burns and bruises)
Can also be chronic (e.g. osteoarthritis)
Tends to respond to conventional analgesics

99
Q

What is neuropathic pain?

A

Pain initiated or caused by a primary lesion or dysfunction in the somato-sensory nervous system
The painful region may not necessarily be the same as the site of injury – pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain)
Almost always a chronic condition (e.g. postherpetic neuralgia [PHN], poststroke pain)
Responds poorly to conventional analgesics

100
Q

What are the differences between acute and chronic pain?

A

Acute pain is physiological, whereas chronic is pathological
Noxious stimuli not needed in chronic, but is in acute
Chronic does not serve a purpose
Acute pain is usually nociceptive pain, chronic can be any

101
Q

What can help the transduction part of the pain pathway?

A

NSAIDs
Ice
Rest
LA blocks

102
Q

What can help the transmission part of the pain pathway?

A 
Nerve blocks
Drugs
>Opioids
>Anticonvulsants
Surgery
103
Q

What can help the perception part of the pain pathway?

A 
Education
	Cognitive behavioural therapy
	Distraction
	Relaxation
	Graded motor imagery
	Mirror box therapy
104
Q

What can help the descending modulation part of the pain pathway?

A 
Placebos
Drugs
>Opioids
>Antidepressants
Surgery
>Spinal cord stimulation

Conditions + definitions (68 decks)

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