Neurology Flashcards
1
Q
Vasovagal syncope pathophysiology
A
Stimulus—> vagus nerve—> PNS Vasodilation of cerebral vessels Decreased pressure in cerebral circulation Hypoperfusion of brain tissue Loss of consciousness
2
Q
Prodrome symptoms vasovagal syncope
A
Hot or clammy Sweaty Heavy Dizzy or light-headed Vision going blurry or dark Headache
3
Q
Signs and symptoms during vasovagal syncope
A
Collateral history
Suddenly losing consciousness and falling to the ground
Unconscious on ground for a few seconds to a minute as blood returns to their brain
Twitching, shaking or convulsion activity
Incontinence
4
Q
Postictal period
A
Prolonged period of confusion, drowsiness, irritability, disorientation
5
Q
Causes of primary syncope
A
Dehydration
Missed meals
Extended standing in warm environment
Vasovagal response to stimulus
6
Q
Secondary causes of syncope
A
Hypoglycaemia Dehydration Anaemia Infection Anaphylaxis Arrhythmias (electrolyte abnormalities) Valvular heart disease Hypertrophic obstructive cardiomyopathy
7
Q
Syncope features
A
Prolonged upright position before the event
Lightheaded before event
Sweating before event
Blurring or clouding of vision before the event
Reduced tone during the episode
Return of consciousness shortly after falling
No prolonged post-ictal period
8
Q
Seizures features
A
Epilepsy aura (smells, tastes, deja vu) before event Head turning or abnormal limb positions Tonic clonic activity Tongue biting Cyanosis Lasts >5 minutes Prolonged post-ictal period
9
Q
Types of seizures
A
Generalised tonic-clonic seizures Focal seizures Absence seizures Atonic seizures Myoclonic seizures Infantile spasms Febrile convulsions
10
Q
Generalised tonic-clonic seizures
A
Loss of consciousness
Tonic: muscle tensing followed by
Clonic: muscle jerking
Tongue biting, incontinence, groaning, irregular breathing
Post-ictal period: confused, drowsiness, irritable or low
11
Q
General tonic-clonic seizures management
A
First line: sodium valproate
Second line: lamotrigine or carbamazepine
12
Q
Focal seizures features
A
Temporal lobes: hearing, speech, memory, emotions Hallucinations Memory flashbacks Deja vu Doing strange things on autopilot
13
Q
Focal seizures management
A
First line: carbamazepine or lamotrigine
Second line: sodium valproate, levetiracetam
14
Q
Absence seizures features
A
Typical in children 4-8 Blank Stares into space Returns to normal abruptly Unaware of surroundings during episode Last 10-20seconds Most patients stop as they get older
15
Q
Absence seizures management
A
First line: sodium valproate or ethosuximide
16
Q
Atonic seizures features
A
Drop attacks Brief lapses in muscle tone <3 minutes Typically begin in childhood Indicative of Lennox-Gastaut syndrome
17
Q
Management of atonic seizures
A
First line: sodium valproate
Second line: lamotrigine
18
Q
Myoclonic seizures features
A
Brief muscle contractions
Sudden jump
Patients awake during episode
Part of juvenile myoclonic epilepsy
19
Q
Myoclonic seizures management
A
First line: sodium valproate
Second line: lamotrigine, levetiracetam, topiramate
20
Q
Lennox-Gastaut syndrome
A
Extension of infantile spasms Onset 1-5 years Atypical abscess, falls, jerks 90% moderate-severe mental handicap EEG: slow spike Ketogenic diet may help
21
Q
Benign rolandic epilepsy
A
Most common in childhood M>F
Paraesthesia (e.g. unilateral face), usually on waking up
22
Q
Juvenile myoclonic epilepsy (Janz syndrome)
A
Onset: teens, F:M = 2:1
Infrequent generalised seizures, often in morning/following sleep deprivation
Daytime absences
Sudden, shock like myoclonic seizures (these may develop before seizures)
Usually good response to sodium valproate
23
Q
Infantile spasms features
A
West’s syndrome Infancy->6months Clusters of full body spasms M>F Flexion of head, trunk, limbs-> extension of arms (Salaam attack); last 1-2secs, repeat up to 50times Progressive mental handicap EEG: hypsarrhythmia Usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cytogenetic Poor prognosis
24
Q
Infantile spasms, West syndrome management
A
Prednisolone
Vigabatrin
25
Investigations epilepsy
EEG, after 2nd tonic-clonic
MRI brain
ECG to exclude heart problems
Blood electrolytes: sodium, potassium, calcium, magnesium
Blood glucose: hypoglycaemia, diabetes
Blood cultures, urine cultures, lumbar puncture
26
When should MRI brain be considered in epilepsy
First seizures in <2 years
Focal seizures
No response to first-line anti-epileptic medications
27
General advice for epilepsy
```
Showers > baths
Cautious with swimming
Cautious with heights
Cautious with traffic
Cautious with heavy, hot or electrical equipment
```
28
Sodium valproate side effects
Teratogenic, contraception advice
Liver damage and hepatitis
Hair loss
Tremor
First line for most except focal seizures
Increases activity of GABA
29
Carbamazepine side effects
Agranulocytosis
Aplastic anaemia
Induces P450 system- many drug interactions
First line for focal seizures
30
Phenytoin Side effects
```
Folate and vitD deficiency
Megaloblastic anaemia (folate deficiency)
Osteomalacia (vitD deficiency)
```
31
Ethosuximide side effects
Night terrors
| Rashes
32
Lamotrigine side effects
Stevens-Johnson syndrome or DRESS syndrome
| Leukopenia
33
DRESS syndrome
Drug reaction with eosinophilia and systemic symptoms
34
Management of seizures
Put patient in safe position
Place in recovery position
Put something soft under head
Remove obstacles that could lead to injury
Make a note of time at start and end
Call ambulance if >5 minutes or first seizures
35
Status epilepticus definition
Seizures >5minutes or
>3 seizures in one hour
>=2 seizures within a 5 minute period without the person returning to normal between them
36
Management of status epileptic in hospital
| Initial management
```
Secure airway
High-concentration oxygen
Assess cardiac and respiratory function
Check blood glucose levels
Gain IV access
IV lorazepam, repeat after 10minutes if seizure continues
```
37
Management of status epilepticus in hospital if seizures persist after initial management
Infusion of IV phenobarbital or phenytoin
Intubation and ventilation
Transfer to ICU
38
Options in community to treat status epilepticus
Buccal midazolam
| Rectal diazepam
39
Febrile seizure definition
Seizure associated with a febrile illness
Not caused by CNS infection
No previous neonatal seizures or previous unprovoked seizure
Not meeting criteria for acute symptomatic seizure
6months-6years
40
Febrile seizures epidemiology
12-18months peak incidence
41
Febrile seizure pathophysiology
Viral infections: URTI, LRTI, otitis media, UTI most common
| Also gastroenteritis and fever post-vaccination associated
42
Febrile seizures risk factors
FH
Socio-economic causes
Seasonal: viruses more common in winter
Zinc and iron deficiency
43
Clinical features of febrile seizures
Fever >38
Age 6months-6 years
Tonic-clonic seizure
Symptoms of infection
44
Simple febrile seizure
<15 minutes
Generalised tonic-clonic
Isolated event- doesn’t recur within the same febrile illness
Post-ictal state: uneventful recovery from seizure
45
Complex febrile seizure
>15 minutes
Focal, or focal with secondary generalisation
Recurrence within 24 hours of the same febrile illness
May suffer from Todd’s paresis
46
Febrile status epilepticus
Subgroup of complex febrile seizures
Duration >30minutes
Multiple seizures lasting 30 minutes with no recovery between each one
47
History of febrile convulsions
```
Has child been vaccinated
Are they at school?
Previous treatment with antimicrobials
Any history of trauma or toxin ingestion
Any family history
Developmental history
```
48
Examination in febrile convulsions
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Find source of infection
External ear examination with auroscope- look for signs of otitis externa or otitis media
Throat examination- for signs of URTI (inflamed tonsils)
Full respiratory examination- for signs of LRTI
Check fontanelles
Brudzinskis or Kernigs sign
Nuchal rigidity (neck stiffness)
Mental status of child
Full neurological examination
Cardiovascular examination
Abdominal examination
Urine dipstick and microscopy
Superficial infective skin lesions
```
49
DD febrile seizures
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CNS infection
Delirium
Syncope
Epilepsy
Intracranial space occupying lesions, brain tumours or intracranial haemorrhage
Electrolyte abnormalities
Trauma
```
50
Febrile convulsions investigations
If child >1
Or symptoms of intracranial infection
```
General observations
Clear source of infection
Bedside testing- urinalysis
Bloods: FBC, CRP, U&E, calcium, glucose, magnesium, blood cultures
Stool cultures
Lumbar puncture
Imaging: CXR
CT/ MRI/ EEG in complex seizures
```
51
Red flags of CNS infection
Complex febrile seizures
History of lethargy, irritability or decreased feeding
Prolonged post-ictal altered consciousness or neurological deficit >1 hour
Any physical signs of meningitis/ encephalitis
Previous/ current treatment with antibiotics which may have masked full clinical presentation of meningitis
Incomplete immunisation in children 6-18months against Haemophilus influenza B and streptococcus pneumoniae
52
Acute management febrile seizure
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A-E
Monitor child and prevent injury
Keep child well-hydrated
Paracetamol or ibuprofen
In-depth explanation
```
53
Treatment febrile seizure >5 minutes
Benzodiazepine rescue
54
Febrile seizures risk factors for recurrence
Age <18 months at onset
Shorter duration of fever before seizure (<1 hour)
Relatively lower grade of fever associated with seizure (<40degrees)
Multiple seizures during the same febrile illness
Day nursery attendance
FH of febrile seizure in a first degree relative
55
Risk of epilepsy after febrile seizure
FH epilepsy
Complex focal seizure
Neurodevelopmental impairment
56
Breath holding spells
```
Breath holding attacks
Involuntary episodes
Trigger: something scaring or upsetting them
Occur 6-18months of age
Not harmful in long term
```
Cyanosis breath holding spells
Pallid breath holding spells
57
Cyanotic breath holding spells
Occur when child is really upset, worked up, crying
Stop breathing after letting out a long cry
Become cyanosis and lose consciousness
Regain consciousness within a minute and start breathing again
Tired and lethargic after an episode
58
Reflex anoxic seizures
Occur when child is startled
Vagus nerve sends strong signals to heart that causes it to stop breathing
Child will suddenly go pale, lose consciousness, seizure-like muscle twitching
<30seconds heart restarts and child becomes conscious again
59
Management of breath holding spells
Treat iron deficiency anaemia
60
Causes of headache in children
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Tension headaches
Migraines
ENT infection
Analgesic headache
Problems with vision
RICP
Brain tumours
Meningitis
Encephalitis
Carbon monoxide poisoning
```
61
Tension headaches features
Mild ache across forehead
Pain/pressure in band-like pattern around head
No visual changes or pulsating sensations
Typically symmetrical
Symptoms in young children:
Quiet, stop playing, turn pale or become tired
Resolve quickly in children compared with adults
Within 30 minutes
62
Triggers for tension headaches
Stress, fear or discomfort
Skipping meals
Dehydration
Infection
63
Management tension headaches
```
Reassurance
Analgesia
Regular meals
Avoid dehydration
Reduce stress
```
64
Migraines types
```
Migraine without aura
Migraine with aura
Silent migraine
Hemiplegic migraine
Abdominal migraine
```
65
Symptoms of migraines
Unilateral
More severe
Throbbing in nature
Take longer to resolve
66
Migraine associations
Visual aura
Photophobia and phonophobia
Nausea and vomiting
Abdominal pain
67
Management of migraines in children
```
Rest, fluids and low stimulus environment
Paracetamol
Ibuprofen
Sumatriptan
Antiemetic, domperidone
```
68
Migraine prophylaxis
Propanolol (avoid in asthma)
Pizotifen (drowsiness SE)
Topiramate: teratogenic
69
Abdominal migraine
```
Young children
Occur before the develop traditional migraines
Central abdominal pain >1 hour
N/v
Anorexia
Headache
Pallor
```
70
Sinusitis
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Headache
Inflammation in sinuses
Facial pain
Tenderness over affected sinuses
Sinusitis resolves within 2-3weeks
Mostly viral
```
71
Causes of neonatal hypotonia
Neonatal sepsis
Werdnig-Hoffman disease (spinal muscular atrophy TY1)
Hypothyroidism
Prader-Willi
Maternal drugs, e.g. benzodiazepines
Maternal myasthenia gravis
72
Neurological conditions causing hypotonia
Central hypotonia:
Cerebral palsy
Brain and spinal cord injury
Serious infections; meningitis, encephalitis
```
Peripheral hypotonia:
Muscular dystrophy
Myasthenia gravis
Spinal muscular atrophy
Charcot-Marie-Tooth disease: affects myelin
```
73
Non-neurological causes of hypotonia
```
Down’s syndrome
Prader-Willi
Tay-Sachs disease
Congenital hypothyroidism
Marfan syndrome and Ehlers-Danlos
Connective tissue disorders
Premature
```
74
Causes of hypotonia in larger life
Multiple sclerosis
| Motor neurone disease
75
Extradural haematoma pathophysiology
Collection of blood between skulls and dura
Caused by low-impact trauma
Collection in temporal region, pterion, middle meningeal artery
Haematoma expands
Uncus of temporal lobe herniates around tentorium cerebelli
Compression of parasympathetic fibres of CN3
Biconvex (or lentiform), hyperdense collection around the brain surface
Limited by suture lines of the skull
76
Extradural haematoma presentation
Loses, briefly regains, loses again consciousness
After low impact head injury
Lucid interval
Fixed and dilated pupil from compression of parasympathetic fibres CN3
77
Management of extradural haematoma
Craniotomy
| Evacuation of haematoma
78
Subdural haematoma pathophysiology
Collection of blood deep to dural layer of meninges
High-impact injury
Bridging veins
Crescent collection on CT
Midline shift or herniation
Shaken baby syndrome in infants as they have fragile bridging veins
79
Subdural haematoma management
Surgical decompression with burr holes
80
Subdural haematoma signs and symptoms
Confusion
Reduced consciousness
Neurological deficit
81
Subarachnoid haemorrhage causes
```
Head injury (traumatic SAH)
Absence of trauma (spontaneous SAH)
Intracranial aneurysm: Berry aneurysm, adult polycystic kidney disease, Ehlers-Danlos, coarctation of aorta
AV malformation
Pituitary apoplexy
Arterial dissection
Mycotic (infective) aneurysm
Perimesencephalic (idiopathic venous bleed)
```
82
Classic presenting feature of SAH
```
Headache: thunderclap
N/V
Meningism
Coma
Seizures
Sudden death
ECG changes: ST elevation
```
83
SAH diagnosis
CT head: acute blood
Lumbar puncture: if CT negative, 12 hours following onset of symptoms to allow for Xa tho chronic to develop
Referral to neurosurgery
CT intracranial angiogram
84
SAH treatment
Craniotomy and clipping
Bed rest
Control BP
Avoid straining to prevent re-bleed
21 days of nimodipine to treat vasospasm, treat with hyper volar is, induced-hypertension, haemodilution
Hydrocephalus is treated with external ventricular drain (CSF diverted into a bag at bedside) or long-term ventriculo-peritoneal shunt
85
Complications of aneurysms SaH
Re-bleeding: most common in first 12 hours, need repeat CT
Vasospasm: delayed cerebral ischaemia, 7-14days after onset
Hyponatraemia: SIADH
Seizures
Hydrocephalus
Death
86
Muscular dystrophy
Genetic conditions that cause gradual weakening and wasting of muscles
87
Types of muscular dystrophy
```
Duchennes muscular dystrophy
Becker’s muscular dystrophy
Myotonic dystrophy
Facioscapulohumeral muscular dystrophy
Oculopharyngeal muscular dystrophy
Limb-girdle muscular dystrophy
Emery-dreifuss muscular dystrophy
```
88
Gowers sign
Technique to stand up from a lying position
Proximal muscle weakness
Pelvic weakness
Use hands on their legs to help them stand up
89
Management of muscular dystrophy
```
No curative treatment
Occupational therapy
Physiotherapy
Medical appliances
Manage complications: spinal scoliosis and heart failure
```
90
Duchennes muscular dystrophy pathophysiology
Caused by defective gene for dystrophin on the X-chromosome
Dystrophin helps hold muscles together at cellular level
X-linked recessive
91
Duchennes muscular dystrophy presentation
```
Boys present at 3-5years
Weakness in muscles around pelvis
Progressive weakness
Eventually all muscles will be affected
Wheelchair bound by teenage years
Life expectancy 25-35
Good management of cardiac and respiratory complications
Associated with dilated cardiomyopathy
Calf pseudohypertrophy
```
92
Duchennes muscular dystrophy management
Oral steroids: slow progression of muscle weakness as much as two years
Creatine supplementation: slight improvement in muscle strength
Genetic trials are ongoing
93
Beckers muscular dystrophy presentation
Similar to Duchennes
Dystrophin gene is less severely affected and maintains some function
Symptoms appear 8-12years
Some patients require wheelchairs in their last 20s or 30s
Others able to walk with assistance into later adulthood
Management similar to Duchennes
94
Features of myotonic dystrophy
Progressive muscle weakness
Prolonged muscle contractions
Cataracts
Cardiac arrhythmias
Unable to let go after shaking hand, unable to release doorknob grip
95
Facioscapulohumeral muscular dystrophy
Usually presents in childhood with weakness around face
Progressing to shoulders and arms
Classic initial symptom: sleeping with eyes initially open, weakness in pursing their lips
Unable to blow their cheeks our without air leaking from their mouth
96
Oculopharyngeal muscular dystrophy
Usually presents in late adulthood
Weakness of ocular muscles (around eyes)
Weakness of pharynx (around throat)
Typically presents with bilateral ptosis, restricted eye movements, and swallowing problems
Muscles around limb girdles are also affected to varying degrees
97
Limb-girdle muscular dystrophy
Usually presents in teenage years
| With progressive weakness around limb girdles (hips and shoulders)
98
Emery-Dreifuss muscular dystrophy
Usually presents in childhood with contracture
Most commonly in the elbows and ankles
Contractures: shortening of muscles and tendons that restrict the range of movement in limbs
Patients also suffer with progressive weakness and wasting of muscles, starting with the upper arms and lower legs
99
Raised intracranial pressure pathophysiology
Normal ICP is 7-15mmHg in adults in the supine position
Cerebral perfusion pressure is the net pressure gradient causing cerebral blood flow to the brain
CPP= mean arterial pressure - ICP
100
RICP causes
```
Idiopathic intracranial hypertension
Traumatic head injuries
Infection: meningitis
Tumours
Hydrocephalus
```
101
RICP features
```
Headache
Vomiting
Reduced level of consciousness
Papilloedema
Cushings trial: widening pulse pressure, bradycardia, irregular breathing
```
102
RICP investigations and monitoring
Neuro imaging: CT/ MRI
Invasive ICP monitoring
Catheter placed into lateral ventricle of brain to monitor the pressure
May also be used to take collect CSF samples and also to drain small amounts of CSF to reduce the pressure
Cut-off of >20mmHg is often used to determine if further treatment is needed to reduce the ICP
103
RICP management
Investigate and treat underlying cause
Head elevation to 30degrees
IV mannitol for osmotic diuresis
Controlled hyperventilation, reduce pCO2-> vasoconstriciton of cerebral arteries-> reduced ICP. Rapid, temporary lowering of ICP
Removal of CSF:
Drain from intraventricular monitor
Repeated lumbar puncture
Ventriculoperitoneal shunt
104
Spinal muscular atrophy
Rare autosomal recessive condition
Progressive loss of motor neurones
Progressive muscular weakness
Affects LMN in spinal cord
105
Spinal muscular atrophy signs
```
LMN signs
Fasciculations
Reduced muscle bulk
Reduced tone
Reduced power
Reduced or absent reflexes
```
106
SMA TY1
Onset in first few months of life
| Usually progressing to death within 2 years
107
SMA TY2
Onset within the first 18 months
| Most never walk, but survive into adulthood
108
SMA TY3
Onset after the first year of life
Most walk without support, but subsequently loose that ability
Respiratory muscles are less affected and life expectancy is close to normal
109
SMA TY4
Onset in 20s
Most will retain ability to walk short distances
May require wheelchair for motility
Everyday tasks can lead to significant fatigue
Respiratory muscles and life expectancy aren’t affected
110
Management of spinal muscle atrophy
MDT management
Physiotherapy: maximising strength in muscles and retaining respiratory function. Splints, braces and wheelchairs can be used to maximise function
Respiratory support with non-invasive ventilation, may be required to prevent hypoventilation and resp failure
SMA TY1: may require a tracheostomy with mechanical ventilation
Percutaneous endoscopic gastrostomy: unsafe swallow
