1
Q
Name 3 types of primary headache
A
No underlying cause
- Migraine
- Tension headache
- Cluster headache
2
Q
Name 2 types of secondary headache
A
Underlying cause
- Meningitis
- Subarachnoid haemorrhage
- Giant cell arteritis
- Idiopathic intracranial hypertension
- Medication overuse headache
3
Q
Give an example of a tertiary headache
A
Trigeminal neuralgia
4
Q
Give 6 questions that are important to ask when taking a history of headache
A
- Time = onset, duration, frequency, pattern
- Pain = severity, quality, site, spread
- Associated symptoms - n/v, photophobia, phonophobia
- Triggers/aggravating/relieving factors
- Response to attack = is medication useful?
- What are the symptoms like between attacks?
5
Q
Give 5 red flags for suspected brain tumour in a patient presenting with a headache
A
- New onset headache and history of cancer
- Cluster headache
- Seizure
- Significantly altered consciousness, memory, confusion
- Papilloedema
- Other abnormal neurological exam
6
Q
How long do migraine attacks tend to last for?
A
Between 4-72 hours
7
Q
Briefly describe the pathophysiology of migraines
A
- Cerebrovascular constriction –> aura, dilation –> headache
- Spreading of cortical depression
- Activation of CN V nerve terminals in meninges and cerebral vessels
8
Q
what are the main triggers of migraines?
A
CHOCOLATE
C - chocolate H - hangovers O - oral contraceptives C - cheese O - orgasms L - lie-ins A - alcohol T - tumult i.e. loud noises E - exercises
9
Q
Describe the pain of a migraine
A
A symptoms:
- Unilateral
- Throbbing
- Moderate/severe pain
- Aggravated by physical activity
10
Q
What other symptoms may a patient with a migraine experience other than pain?
A
B symptoms:
- Nausea
- Photophobia
- Phonophobia
- Aura
11
Q
What is a prodrome for migraines?
A
Precedes migraine by hours-days
- yawning
- food cravings
- changes in sleep, appetite or mood
12
Q
what is a migraine aura?
A
Precedes migraine attacks and can be a variety of symptoms
- Visual = lines, dots, zig-zags
- somatosensory = paraesthesia, pins and needles
Dysphagia
Ataxia
13
Q
what are the differential diagnoses for a migraine?
A
- Other headache type
- Hypertension
- TIA
- Meningitis
- Subarachnoid haemorrhage
14
Q
What is the diagnostic criteria for a migraine?
A
- classified as with or without aura
- at least 2 of:
- unilateral pain (usually 4-72hrs)
- throbbing-type pain
- moderate > severe intensity
- motion sensitivity
plus at least 1 of:
- nausea/vomiting - photophobia/phonophobia
there must also be a normal examination and no attributable cause
15
Q
How can migraines be subdivided?
A
- Episodic with (20%)/without (80%) aura
2. Chronic migraine
16
Q
what is the treatment for migraines
A
- triptans e.g. sumatriptan
- NSAIDs e.g. naproxen
- anti-emetic e.g. prochlorperazine
- AVOID opioids and ergotamine
17
Q
How does triptan work?
A
Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain
18
Q
How long do tension headaches usually last for?
A
From 30 minutes to 7 days
19
Q
what are tension headaches?
A
most common chronic daily and recurrent headache
Can be episodic <15 days/month or chronic >15 days/month (for at least 3 months)
There is no known organic cause, however a number of triggers exist
20
Q
Would a patient with a tension headache experience any other symptoms other than pain?
A
NO
Nausea, photophobia and photophobia would NOT be associated
21
Q
How do you treat a tension headache?
A
avoidance of triggers and stress relief
symptomatic relief:
- aspirin
- paracetamol
- ibuprofen / diclofenac
- AVOID OPIOIDS
limit analgesics to no more than 6 days per month to reduce risk of medication-overuse headaches
22
Q
what is the clinical presentation of a cluster headache?
A
- rapid onset excruciating pain, classically around the eye (or temples/forehead)
- pain is unilateral and localised.
- pain rises to crescendo over a few minutes and lasts for 15-160 minutes, once or twice daily (usually around the same time)
- ipsilateral autonomic features:
- watery/bloodshot eye
- facial flushing
- rhinorrhoea (blocked nose)
- miosis (pupillary constriction) +/- ptosis
23
Q
How can cluster headaches be subdivided?
A
Episodic = >2 cluster periods lasting 7 days - 1 year separated by pain free periods lasting >1 month Chronic = attack occur for >1 year without remission or remission lasting <1 month
24
Q
How long do cluster headaches tend to last?
A
Between 15 minutes and 3 hours
Mostly nocturnal
25
what is the treatment for cluster headaches?
FOR ACUTE ATTACKS:
- analgesics are unhelpful
- 15L 100% O2 for 15mins via non-rebreather mask
- triptans e.g. sumatriptan
26
What is the most common type of secondary headache?
Medication overuse headache - episodic headache becomes daily chronic headache
27
Describe the pain of trigeminal neuralgia
1. Unilateral face pain
2. Severe intensity
3. Electric shock like, shooting, stabbing or sharp
4. No radiation beyond the trigeminal distribution
28
Describe the epidemiology of trigeminal neuralgia
Peak age = 50-60 years
| Women > men
29
Give 3 causes of trigeminal neuralgia
1. Compression of trigeminal nerve by a loop of vein or artery
2. Aneurysms
3. Meningeal inflammation
4. Tumours
30
How long does the pain associated with trigeminal neuralgia usually last for?
A few seconds
| Maximum 2 minutes
31
What is the treatment for trigeminal neuralgia?
Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery
32
What features might be present in the history of a headache that make you suspect meningitis?
1. Pyrexia
2. Photophobia
3. Neck stiffness
4. Non-blanching purpura rash
33
At what level is a lumbar puncture done and why is an LP done?
L3/4 or L4/5
| To obtain a CSF sample
34
What does a small response on an nerve conduction study suggest?
There is axon loss
35
What does a slow response on an nerve conduction study suggest?
There is myelin loss
36
Define encephalopathy
Reduced level of consciousness/diffuse disease of brain substance
37
Define neuropathy
Damage to one or more peripheral nerve, usually causing weakness and/or numbness
38
Define myelitis
Inflammation of the spinal cord
39
Define meningitis
Infection and inflammation of the meninges of the brain
it is a notifiable disease
40
Name 3 bacterial organisms that cause meningitis in adults
1. N. meningitidis
2. S. pneumoniae
3. H. influenzae
41
Name 2 bacterial organisms that cause meningitis in neonates
1. E.coli
| 2. Group B strep - strep agalactiae
42
Name 3 viruses that can cause meningitis
1. Enterovirus (most common viral)
2. HSV
3. CMV
4. Varicella zoster virus
43
Name 2 organisms that can cause meningitis in immunocompromised patients
1. CMV
2. Cryptococcus
3. TB
4. HIV
5. herpes simplex
44
Give the main triad of symptoms of meningitis
Headache + neck stiffness + fever
45
what are the symptoms of meningitis
1. Neck stiffness
2. Photophobia
3. Papilloedema (due to increased ICP)
4. Petechial non-blanching rash
5. Headache
6. Fever
7. Decreased GCS
46
what are the signs of meningitis
Kernig's sign = unable to straighten leg more than 135 degrees without pain when hip is flexed to 90 degrees
Brudzinski's sign = severe neck stiffness cause hip and knees to flex when neck is flexed
47
How would you describe the rash associated with meningococcal sepsis?
Petechial non-blanching rash
48
What investigations might you do in someone you suspect has meningitis?
1. Blood cultures (pre LP)
2. Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
3. Lumbar puncture (contraindicated with raised ICP)
4. CT head - exclude lesions
5. Throat swabs - bacterial and viral
49
What is the treatment of bacterial meningitis?
- ABCDE + support
- Empirical therapy = IV Benzylpenicillin
Assess GCS
- First line = Ceftriaxone / Cefotaxime
- Add IV Benzylpenicillin for rash
- Penicillin allergy = Chloramphenicol
- Immunocompromised ( Risk of Listeria) = Amoxicillin / Ampicillin
oral dexamethasone to reduce cerebral oedema
50
What is the treatment of viral meningitis?
Watch and wait
| acyclovir
51
What is the treatment for meningococcal septicaemia?
IV BENZYLPENICILLIN (in community)
IV CEFOTAXIME (in hospital)
52
What can be given as prophylaxis against meningitis?
IV CIPROFLOXACIN (all ages and pregnancy) and IV RIFAMPICIN (all ages but NOT pregnancy)
53
For which bacteria is meningitis prophylaxis effective against?
N. meningitidis
54
Give 4 potential adverse effect of a lumbar puncture
1. Headache
2. Paraesthesia
3. CSF leak
4. Damage to spinal cord
55
What investigations would you do on a CSF sample?
Protein and glucose levels
MCS
Bacterial and viral PCR
56
When would you do a CT before an LP?
```
>60
Immunocompromised
History of CNS disease
New onset/recent seizures
Decreased GCS
Focal neurological signs
Papilloedema
```
57
What is the colour of the CSF in someone with a bacterial infection?
Cloudy (normally it is clear)
58
Give 4 reasons why a lumbar puncture might be contraindicated
1. Thrombocytopenia
2. Delay in Abx admin
3. Signs of raised ICP
4. Unstable cardio or resp systems
5. Coagulation disorder
6. Infections at LP site
7. Focal neurological signs
59
Define encephalitis
Infection and inflammation of the brain parenchyma
60
In what group of people is encephalitis common?
Immunocompromised
| the infections are most frequent in children and elderly
61
What area of the brain does encephalitis mainly affect?
Frontal and temporal lobes
62
what are the viral causes of encephalitis
1. Herpes simplex (most common)
2. CMV
3. Epstein Barr
4. varicella zoster
5. HIV
6. measles
7. mumps
63
what are the non-viral causes of encephalitis
1. Bacterial meningitis
2. TB
3. Malaria
4. Lyme's disease
64
Name the main triad of symptoms of encephalitis
Fever + headache + altered mental state
65
what is the clinical presentation of encephalitis?
begins with features of viral infection:
- fever, headaches, myalgia, fatigue, nausea
progresses to:
- personality & behavioural changes
- decreased consciousness, confusion, drowsiness
- focal neurological deficit - hemiparesis, dysphagia
- seizures
- raised ICP and midline shift
- coma
66
What would the LP show from someone with encephalitis?
- CSF shows elevated lymphocyte count
| - viral detection by CSF PCR
67
What investigations might you do on someone with encephalitis?
- MRI - shows areas of inflammation, may be midline shifting
- EEG - periodic sharp and slow wave complexes
- lumbar puncture
- blood and CSF serology
68
What is the treatment for encephalitis?
- IV Acyclovir immediately - even before investigation results
- Primidone = anti-seizure medication if needed
- IV benzylpenicillin if meningitis is suspected
69
How does herpes zoster occur?
Reactivation of varicella zoster virus, usually within the dorsal root ganglia
70
where does herpes zoster commonly occur?
- thoracic nerves
- ophthalmic division of trigeminal nerve
- cervical, lumbar and sacral nerve roots
71
what is the clinical presentation of herpes zoster?
- Pain and paraesthesia in dermatomal distribution priced rash for days
- Malaise, myalgia, headache and fever can be present
- Can be over a week before eruption appears
- Rash - consists of papules and vesicles
RESTRICTED to SAME DERMATOME:
• Neuritic pain
• Crust formation and drying occurs over the next week with resolution in 2-3 weeks
• Patients are infectious until lesions are dried
• RASH DOES NOT EXTEND OUTSIDE DERMATOME
72
Describe the treatment for herpes zoster
Antiviral therapy within 72 hours of rash onset - ACYCLOVIR or VALICICLOVIR or FAMCICLOVIR
Analgesia - IBUPROFEN
73
Briefly describe the pathophysiology of herpes zoster
Latent virus is reactivated in dorsal root ganglia --> travels down affected nerve via sensory root in dermatomal distribution --> perineural and intramural inflammation
74
What dermatome is herpes zoster most likely to affect?
Thoracic nerves
| Then ophthalmic division of trigeminal
75
Give 2 complications of herpes zoster
1. Ophthalmic branch of trigmeinal = damages sight
| 2. Post herpetic neuralgia - pain lasts >4 months after
76
What is MS?
A chronic autoimmune, T-cell mediated inflammatory condition of the CNS characterised by multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years
77
Briefly describe the pathophysiology of MS
- Autoimmune inflammation causes CD4 mediated destruction of oligodendrocytes
- This causes demyelination of CNS neurones. The myelin sheath regenerates but is less efficient
- Repeated demyelination leads to axonal loss and incomplete recovery between attacks
- Poor demyelination healing results in relapsing and remitting symptoms
- Multiple areas of sclerosis (scar tissue) form along neurones which slow/block conduction of signals thus impairing movement and/or sensation
78
What is MS characterised by?
Disseminated in space and time
Hypercellular plaque formation
BBB disruption
79
what are the different types of MS?
1. Relapsing remitting (80%)
2. secondary progressive MS
3. primary progressive MS
80
what are the causes/risk factors of MS?
```
Unknown
Environment and genetic components
- exposure to EBV in childhood
- low levels of sunlight and vitamin D
- female
- white
- living far from equator
```
81
Describe the epidemiology of MS
Presenting between 20-40 y/o
Females > Males
More common in white populations
82
what are the symptoms of MS?
TEAM
- Tingling
- Eye = optic neuritis
- Ataxia
- Motor - spastic paraparesis, pyramidal weakness (UL = extensors, LL = flexors)
- swallowing disorders
- bladder incontinence
- dizziness, falls
- constipation
- fatigue
- cognitive impairment, depression
83
what are the signs of MS?
- Lhermitte sign - electric jolt felt down the spine when flexing neck
- Uhthoff phenomenon - symptoms worse with heat, e.g. hot bath/exercise
84
What can exacerbate the symptoms of MS?
Heat (e.g. a warm shower)
85
Name 3 differential diagnosis's of MS
1. SLE
2. Sjogren's
3. AIDS
4. Syphilis
86
What investigations might you do in someone to see if they have MS?
● Symptoms must be disseminated in time and space
MRI = gold standard
- GD-enhancing plaques
● Lumbar puncture = oligoclonal IgG bands
● Bloods = rule out other causes
87
What is the diagnostic criteria for MS?
>2 CNS lesions disseminated in time and space (>2 attack affected different parts of the CNS)
88
Describe the non-pharmacological treatment for MS
must notify DVLA
Regular exercise, smoking and alcohol cessation, low stress lifestyle
Psychological therapies
Speech therapists
Physio and OR
89
Describe the pharmacological treatment for MS
acute relapse
- steroids = IV METHYLPREDNISOLONE
chronic/frequent relapse
- biological - SC BETA INTERFERON (contraindicated in pregnancy)
- DMARDs - IV alentuzumab, IV natalizumab
90
What symptomatic treatments can you give to those with MS?
Spasticity
- BACLOFEN (GABA analogue, reduces Ca2+ influx)
- TIZANIDINE (alpha-2 agonist)
- BOTOX INJECTION (reduces ACh in neuromuscular junction)
urinary incontinence = catheterisation
incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs
91
What medication might you give to someone to reduce the relapse severity of MS?
Short course steroids - methylprednisolone
92
Define epilepsy
Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures
93
Define epileptic seizure
Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excess, hypersynchronous neuronal discharge in the brain
94
Give 5 causes of epilepsy
1. Idiopathic (2/3)
2. cortical scarring
3. tumour
4. stroke
5. alzheimers dementia
6. alcohol withdrawal
95
What 2 categories can epileptic seizures be broadly divided into?
1. Focal epilepsy - only one portion of the brain is involved
2. Generalised epilepsy - whole brain is affected
96
Give 2 examples of focal epileptic seizures
1. Simple partial seizures
| 2. Complex partial seizures
97
Give 3 examples of generalised epileptic seizures
1. Absence seizures
2. Tonic-clonic seizure (grand mal)
3. Myoclonic seizure (isolated jerking)
4. Atonic seizure (floppy)
5. tonic seizure (high tone)
6. clonic seizure (jerking)
98
what are the different components of an epileptic seizure?
- prodrome
- aura
- post-ictal
99
What is aura?
- Part of the seizure where the patient is aware & often precedes other manifestations
- Eg. strange feelings in gut, déjà vu, strange smells, flashing lights
- Often implies a partial seizure
100
If a patient experienced epilepsy with aura, what other symptoms would they get?
Strange feeling in gut
Deja vu
Strange smells
Flashing lights
101
Name 3 post-ictal symptoms
1. Headache
2. Confusion
3. Myalgia
4. Temporary weakness (focal seizure)
102
What is the diagnostic criteria for epilepsy?
At least 2 or more unprovoked seizures occurring >24 hours apart
One unprovoked seizure + probability of future seizures
Epileptic syndrome diagnosis
103
What is the treatment for focal epileptic seizures?
```
Lamotrigine = 1st line
Carbamazepine = 2nd line
```
104
How do lamotrigine and Carbamazepine work?
Inhibit pre-synaptic Na+ channels so prevent axonal firing
105
What is the treatment for generalised epileptic seizures?
Sodium valproate = 1st line
| Lamotrigine = 2nd line
106
How does sodium valproate work?
Inhibits voltage gated Na+ channels and increases GABA production
107
What medication can control seizures?
Diazepam or lorazepam
108
What possible surgery could you do to treat epilepsy?
Vagal nerve stimulation
| Resection of affected area
109
Give 4 potential side effects of anti-epileptic drugs (AED's)
1. Cognitive disturbances
2. Heart disease
3. Drug interactions
4. Teratogenic
110
Give 4 differential diagnosis's of epilepsy
1. Syncope
2. Non-epileptic seizure
3. Migraine
4. Hyperventilation
5. TIA
111
Define syncope
Insufficient blood or oxygen supply to the brains causes paroxysmal changes in behaviour, sensation and cognitive processes
Caused by sitting/standing
5-30 seconds duration
112
Define non-epileptic seizure
Mental processes associated with psychological distress causes paroxysmal changes in behaviour, sensation and cognitive processes
1-20 minute duration
Closed eyes and mouth
113
A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?
A non-epileptic seizure
114
A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?
An epileptic seizure
115
A patient complains of having a 'black out'. They tell you that before the 'black out' they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?
This is likely to be due to a blood circulation problem e.g. syncope
116
Name 3 intra-cranial haemorrhages
1. Sub-arachnoid haemorrhage
2. Sub-dural haemorrhage
3. Extra-dural haemorrhage
117
What can cause a subarachnoid haemorrhage?
- Traumatic injury
- Berry aneurysm rupture
(70-80%) - at common points round Circle of Willis
- Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins
- Idiopathic (15-20%)
118
Give 3 risk factors for a subarachnoid haemorrhage
Hypertension
Known aneurysm
Previous aneurysmal SAH
Smoking
Alcohol
Family history
Bleeding disorders
- associated with berry aneurysms:
- Polycystic Kidney Disease
- Coarctation of aorta
- Ehlers-Danlos syndrome & Marfan syndrome
119
Briefly describe the pathophysiology of a subarachnoid haemorrhage
1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
2. raised ICP - fast flowing arterial blood is pumped into the cranial space
3. space occupying lesion - puts pressure on the brain
4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
5. vasospasm - bleeding irritates other vessels -> ischaemic injury
120
what are the symptoms of a subarachnoid haemorrhage?
1. sudden onset excruciating headache - thunderclap, worst headache, typically occipital
2. sentinel headache - before main rupture, sign of warning leak
3. nausea
4. vomiting
5. collapse
6. loss of/depressed consciousness
7. seizures
8. vision changes
9. coma - can last for days
121
what are the signs of a subarachnoid haemorrhage?
signs of meningeal irritation
1. Kernig's sign (can't straighten leg past 135 degrees)
2. neck stiffness
3. Brudzinski's sign (Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed)
- retinal, subhyaloid and vitreous bleeds
- worse prognosis
- with/without papilloedema
- neurological signs - e.g. 3rd nerve palsy
- increased BP
122
What investigations might you do to see if someone has a subarachnoid haemorrhage?
1. urgent Head CT = star pattern (diagnostic)
2. Lumbar Puncture = xanthochromia -> RBC breakdown (only if normal ICP and after 12 hrs)
3. MR/CT angiography - to establish source of bleeding
123
Describe the treatment for a subarachnoid haemorrhage
- NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
- surgery = endovascular coiling
- IV fluids - maintain cerebral perfusion
- ventricular drainage for hydrocephalus
124
Give 3 possible complications of a subarachnoid haemorrhage
1. Rebleeding (common = death)
2. Cerebral ischaemia
3. Hydrocephalus
4. Hyponatraemia
125
What can cause a subdural haematoma?
Head injury --> vein rupture
126
Describe the pathophysiology of a subdural haematoma
1. bleeding from bridging veins into the subdural space forms a haematoma
2. then bleeding stops
3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges
4. gradual rise in ICP over weeks
5. midline structures shift away from side of clot - causes tentorial herniation and coning
127
What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?
Clot starts to break down and there is massive increase in oncotic pressure --> water is sucked up by osmosis into the haematoma
128
Give 3 risk factors of a subdural haematoma?
1. Elderly - brain atrophy, dementia
2. Frequent falls - epileptics, alcoholics
3. Anticoagulants
4. babies - traumatic injury ("shaking baby syndrome")
129
what are the signs and symptoms of a subdural haematoma?
SYMPTOMS:
1. Fluctuating GCS
2. Headache
3. Confusion - may fluctuate
4. Drowsiness
5. physical and intellectual slowing
6. personality change
7. unsteadiness
SIGNS
1. raised ICP - seizures
2. localising neurological signs (unequal pupils, hemiparesis)
130
Name 3 differential diagnosis's of a subdural haematoma
1. Stroke
2. Dementia
3. CNS masses (tumour vs abscess)
131
What are the investigations for a subdural haematoma?
- CT SCAN:
- crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
- unilateral
- shows midline shift
- MRI SCAN
132
What is the treatment for a subdural haematoma?
SURGERY
- 1* = irrigation via burr-hole craniostomy
- 2* = craniotomy
IV MANNITOL - to reduce ICP
address cause of trauma
133
What can cause an extradural haematoma?
Traumatic head injury resulting in a skull fracture (often temporal bone) --> middle meningeal artery rupture --> bleed
134
what is the pathophysiology of extradural haematoma?
Blood accumulates rapidly in the space between the dura and the skull (over minutes to hours)
After a lucid interval there is:
- rapid rise in ICP
- pressure on the brain
- midline shift
- tentorial herniation
- coning
135
what is the clinical presentation of an extradural haematoma?
- initial injury followed by lucid period
- period of rapid deterioration
- rapid decline in GCS
- increasing severe headache
- vomiting
- seizures
- hemiparesis
- coma
- UMN signs
- ipsilateral pupil dilation
- bilateral limb weakness
- deep and irregular breathing - due to coning
- late signs = bradycardia and raised BP
- death from respiratory arrest
136
What investigations might you do to see if someone has an extradural haematoma? What are the results
CT SCAN
- lens shaped haematoma = LEMON SHAPE
- doesn't cross suture lines
- shows midline shift
SKULL X-RAY
- fracture lines may be seen
LP is CONTRAINDICATED
137
What do the ventricles do to prolong survival in someone with an extradural haematoma?
Get rid of CSF to prevent rise in ICP
138
What is the treatment for an extradural haematoma?
STABILISE PATIENT
URGENT SURGERY
- clot evacuation
- ligation of bleeding vessel
IV MANNITOL
- to reduce ICP
airway care
- intubation and ventilation
139
Give 3 differences in the presentation of a patient with a subdural haematoma in comparison to an extradural haematoma
1. Time frame: extra-dural symptoms are more acute
2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma
3. CT: extra-dural haematoma will have a lens appearance whereas subdural will have a crescent shaped haematoma
140
Define weakness
Impaired ability to move a body part in response to will
141
Define paralysis
Ability to move a body part in response to will is completely lost
142
Define ataxia
Willed movements are clumsy, ill-direction or uncontrolled
143
Define involuntary movements
Spontaneous movement independent of will
144
Define apraxia
Disorder of conscious organised pattern of movement or impaired ability to recall acquired motor skills
145
Give 3 things that modulate LMN action potential transmission to effectors
1. Cerebellum
2. Basal ganglia
3. Sensory feedback
146
Give 3 disease that are associated with motor neurone damage
1. Motor neurone disease
2. Spinal atrophy
3. Poliomyelitis
4. Spinal cord compression
147
Give 3 pathologies that are associated with ventral spinal root damage
1. Prolapsed intervertebral disc
2. Tumours
3. Cervical or lumbar spondylosis
148
Name a disease associated with NMJ damage
Myasthenia Gravis
149
Describe the pyramidal pattern of weakness in the upper limbs
Flexors are stronger than extensors
150
Describe the pyramidal pattern of weakness in the lower limbs
Extensors are stronger than flexors
151
What is a UMN?
A neurone that is located entirely in the CNS
| Its cell body is located in the primary motor cortex
152
Give 3 causes of UMN weakness
1. MS
2. Brain tumour
3. Stroke
4. MND
153
Give 4 sites of UMN damage
1. Motor cortex lesions
2. Internal capsule
3. Brainstem
4. Spinal cord
154
Give 4 signs of UMN weakness
1. Spasticity
2. Increased muscle tone (hypertonia)
3. Hyper-reflexia
4. Positive babinski's reflex
155
Give 4 signs of LMN weakness
1. Flaccid
2. Hypotonia
3. Hypo-reflexia
4. Muscle atrophy
5. Fasciculation's
156
Define motor neurone disease (MND)
A group of neuro degenerative disorders that selectively affect the motor neurons
Most in the anterior horn, cells of the spinal cord and the motor cranial nuclei
There are no sensory problems
157
Does MND affect UMN or LMN?
Both UMN and LMN can be affected
158
Does MND affect eye movements?
Never affects eye movements (clinical feature of myasthenia gravis)
159
Does MND cause sensory loss or sphincter disturbance?
No (clinical feature of MS)
160
What is the epidemiology of MND?
- relatively uncommon
- males > females (3:2)
- often fatal in 2-4 years
161
What is the clinical presentation of MND?
- results in mixed UMN and LMN presentation (LMN symptoms predominate)
- wrist drop/foot drop
- change in appearance of hands - wasting
- gait disorders/tendencies to trip
- excessive fatigue
162
What investigations might you do in someone you suspect to have MND?
```
Head/spine MRI
Blood tests = muscle enzymes, autoantibodies
Nerve conduction studies
EMG
Lumbar Puncture
```
163
What is the diagnostic criteria for MND?
LMN + UMN signs in 3 regions
El Escorial criteria
1. Presences of LMN and UMN degeneration and progressive history
2. Absence of other disease processes
164
What is the treatment for MND?
- MDT care
- anti-glutaminergic drugs - ORAL RILUZOLE - Na+ channel blocker, inhibits glutamate release
- Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
- Dysphagia: NG tube
- Spasms: ORAL BACLOFEN
- Non-invasive ventilation
- Analgesia e.g. NSAIDs - DICLOFENAC
165
Give 3 limb onset symptoms of MND
1. Weakness
2. Clumsiness
3. Wasting of muscles
4. Foot drop
5. Tripping
166
Give 3 respiratory onset symptoms of MND
1. Dyspnoea
2. Orthopnoea
3. Poor sleep
167
Would you do a LP in a patient that has a raised ICP?
NO
| LP is contraindicated if they have a raised ICP due to the risk of coning
168
Give 4 signs of raised ICP
1. Papilloedema
2. Focal neurological signs
3. Loss of consciousness
4. New onset seizures
169
What is the treatment for raised ICP?
Osmotic diuresis with mannitol
170
Explain the ICP/volume curve
Volume increase --> ICP plateau (compensate) --> rapid ICP increase
171
What are the 4 cardinal presenting symptoms of brain tumours?
1. Raised ICP --> headache, decrease GCS, n+v, papilloedema
2. Progressive neurological deficit --> deficit of all major functions (motor, sensory, auditory, visual) + personality change
3. Epilepsy
4. lethargy/tiredness - caused by pressure on brainstem
172
You ask a patient with a brain tumour about any facts that aggravate their headache, what might they say?
1. Worse first thing in the morning
| 2. Worse when coughing, straining or bending forward
173
Name 2 differential diagnosis's for a brain tumour
1. Aneurysm
2. Abscess
3. Cyst
4. Haemorrhage
5. Idiopathic intracranial hypertension
174
What investigations might you do in someone you suspect to have a brain tumour?
CT/MRI head and neck
Biopsy - via burr hole
blood tests - FBC, U&E, LFTs, B12
LP = CONTRAINDICATED (high ICP)
175
Where might secondary brain tumours arise from?
1. non-small cell lung cancer
2. small cell lung cancer
3. breast
4. melanoma
5. renal cell carcinoma
6. GI
176
Describe the treatment for secondary brain tumours
1. surgery - if age <75yrs
2. radiotherapy
3. chemotherapy
4. palliative therapy
177
From what cells to primary brain tumours originate?
Glial cells (gliomas)
- Astrocytoma (85-90%)
- Oligodendroglioma
Other primary = meningioma, schwannoma, medulloblastoma
178
Describe the WHO glioma grading
Grade 1 = benign paediatric tumour
Grade 2 = Pre-malignant tumour (benign)
Grade 3 = 'Anaplastic astrocytoma' (cancer)
Grade 4 = Glioblastoma multiforme (GBM) - malignant
179
Describe the epidemiology of grade 2 gliomas
Disease of young adults
180
Give 3 causes of grade 2 glioma deterioration
1. Tumour transformation to a malignant phenotype
2. Progressive mass effect due to slow tumour growth
3. Progressive neurological deficit form functional brain destruction by tumour
181
Describe the common pathway to a GBM (grade 4 brain tumour)
Initial genetic error of glucose glycolysis --> Isocitrate Dehydrogenase 1 mutation --> excessive build up of 2-hydroxyglutarate --> genetic instability of glial cells --> grade II-IV glioma transform into glioblastoma
182
Give 5 good prognostic factors for GBM
1. <45 y/o
2. Aggressive surgical therapy
3. Good performance post-surgery
4. Tumour that has transformed from previous lower grade tumour
5. MGMT mutant - will respond will to chemo
183
Describe the treatment for GBM
1. Resective surgery
2. Adjuvant chemotherapy with Temozolomide
3. Dexamethasone - reduces tumour inflammation/oedema
4. anticonvulsants - oral carbimazepine
5. palliative care
184
How does Temozolomide work in treatment for GBM?
Methylates guanine in DNA making replication impossible
| MGMT gene reverses it = tumour resistance
185
Define dementia
A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language
There is a progressive decline in cognitive function
186
Describe the epidemiology of dementia
Rare <55
10% of people >65
20% of people >80
187
Give 3 causes of dementia
1. Alzheimer's disease (50%)
2. Vascular dementia (25%)
3. Lewy body dementia (15%)
4. Fronto-temporal (Pick's)
5. Huntington's
6. Liver failure
7. Vitamin deficiency - B12 or folate
188
Give 3 risk factors of dementia
1. Family history
2. Age
3. Down's syndrome
4. Alcohol use, obesity, HTN, hyperlipidaemia, DM
5. Depression
6. ? Head injury
189
Describe the pathophysiology of Alzheimer's disease
Degeneration of temporal lobe and cerebral cortex, with cortical atrophy
Accumulation of beta-amyloid peptide --> progressive neuronal damage, neurofibrillary tangles, increase in number of amyloid places and loss of ACh
190
what is the clinical presentation of Alzheimer's Disease
```
● Memory - episodic and semantic
● Language - difficulty understanding or
finding words
● Attention and concentration issues
● Psychiatric changes, e.g. withdrawal,
delusions
● Disorientation, e.g. time and surroundings
```
191
Give 2 histological signs of Alzheimer's dementia
1. Plagues of amyloid
| 2. Neurofibrillary tangles
192
25% of all patients with Alzheimer's Disease will develop what?
Parkinsons
193
What does vascular dementia often present with?
● Characterised by stepwise progression - Periods of stable symptoms, followed by a sudden increase in severity
● Presentation varies massively but can include:
- Visual disturbances,
- UMN signs (e.g. muscle weakness, overactive reflexes, clonus),
- attention deficit,
- depression,
- incontinence,
- emotional disturbances
○ If infarct was subcortical, then expect to see dysarthria and parkinsonisms
194
Describe the pathophysiology of Lewy body dementia
● Characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex
● Also see substantia nigra depigmentation and amyloid deposits
195
what are the clinical features of Lewy body dementia
● Dementia is often presented initially
○ Memory loss, spatial awareness difficulties,
loss of cognitive function
● Parkinsonisms, e.g. tremor, rigidity, change in gait
● Visual hallucinations
● Sleep disorders, restless leg syndrome
196
Frontal lobe atrophy is seen on an MRI, what kind of dementia is this patient likely to have?
Fronto-temporal
| = frontal and temporal lobe atrophy
197
Give 3 symptoms of Fronto-temporal dementia
● Onset tends to be insidious and progressive
● Present with 3 main symptoms:
○ Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning
○ Progressive aphasia, e.g. slow, difficult speech, grammatical errors
○ Semantic dementia, e.g. loss of vocabulary, problems understanding
198
What is functional memory dysfunction?
Acquired dysfunction of memory that significantly affects a person's professional/private life in absence of an organic cause
199
How could you determine whether someone has functional memory dysfunction or a degenerative disease?
When asked the question 'when was the last time your memory let you down?', someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer
200
What investigations can you do in primary care to determine whether someone might have dementia?
1. Good history of symptoms
2. 6 item cognitive impairment test (6CIT)
3. Blood tests - FBC, liver biochemistry, TFTs, vitamin B12 and folate
4. Mini mental state examination = screening
201
What questions are asked in 6CIT?
1. What year is it?
2. What month is it?
3. Give an address with 5 parts
4. Count backwards from 20
5. Say the months of the year in reverse
6. Repeat the address
202
What secondary care investigation can you do to investigate a dementia diagnosis?
Brain MRI - where and extent of atrophy
Brain function tests = PET, SPECT and functional MRI
Brain CT
Myeloid and tau histopathology
203
Name the staging system that classifies the degree of pathology in AD
Braak staging
Stage 5/6 = high likelihood of AD
Stage 3/4 = intermediate likelihood
Stage 1/2 = low likelihood
204
Give 3 ways in which dementia can be prevented
1. Smoking cessation
2. Healthy diet
3. Regular exercise
4. Low alcohol
5. Engaging in leisure activités
205
What support should be offered to patients with dementia?
Social suport
Cognitive support
Specialist memory service
206
What medications might you use in someone with dementia?
```
Acetylcholinesterase inhibitors - increase ACh = donepezil, rivastigmine
Control BP (ACEi) to reduce further vascular damage
```
207
What is myasthenia gravis?
Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction
208
what is the pathophysiology behind myasthenia gravis?
Autoantibodies (IgG) attach to ACh receptor and destroy them --> fewer action potentials fire --> muscle weakness and fatigue
209
what are the causes/risk factors for myasthenia gravis?
If <50 = associated with other AI conditions (pernicious anaemia, SLE, RA) and more common in women
If >50 = associated with thymic atrophy, thymic tumour, SLE and RA and more common in men
210
what are the clinical features of myasthenia gravis?
1. Muscle weakness
2. Increasing muscular fatigue
3. Ptosis
4. Diplopia
5. Myasthenic snarl
6. Tendon reflexes normal but fatigable
```
● Weakness is more marked in proximal muscles
● Weakness might be seen in:
○ Small muscle of the hands
○ Deltoid and triceps muscles
○ Bulbar muscles
○ Muscles involved in chewing
● No muscle wasting, sensation is unimpaired
● Seizures can occur
```
211
What muscle groups are affected in myasthenia gravis?
muscle groups affected in order:
- extra-ocular
- bulbar - chewing and swallowing
- face
- neck
- trunk
212
What can weakness due to myasthenia gravis be worsened by?
```
Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs (opiates, BB, gentamicin, tetracycline)
```
213
What investigations might you do to see if someone has myasthenia gravis?
- mostly clinical examination
- positive tensilon test
- anti-AChR antibodies
- TFTs
- EMG
- CT of thymus
- crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis
214
Give 3 possible differential diagnosis's for myasthenia gravis
1. MS
2. Hyperthyroidism
3. Acute Guillain-Barre syndrome
4. Lamert-Eaton myasthenia syndrome
215
What is treatment for myasthenia gravis?
Anti-cholinesterase = pyridostigmine
Immunosuppression = prednisolone (with alendronate - bisphosphonate)
Steroids can be combined with azathioprine or methotrexate
Thymectomy
216
When is a thymectomy considered as a treatment for myasthenia gravis?
Onset <50 y/o and it is poorly controlled
217
Give a complication of myasthenia gravis
Myasthenic crisis
Weakness of respiratory muscle during relapse
Treatment = plasmapheresis and IV immunoglobulin
218
Define Parkinson's disease
Degenerative movement disorder caused by a reduction in dopamine in the pars compacta of the substantia nigra
219
what is the pathway of dopamine production?
Tyrosine --> L-dopa --> Dopamine
220
Describe the pathophysiology of Parkinson's disease
destruction of dopaminergic neurones (in substantia nigra) --> reduced dopamine supply --> thalamus inhibits --> decrease in movement + symptoms
Lewy body formation in basal ganglia
221
What is the 3 cardinal symptoms for Parkinsonism?
resting tremor
rigidity
bradykinesia
postural instability
222
what are the clinical features of Parkinson's disease
● Often an insidious onset
- impaired dexterity,
- fixed facial expressions,
- foot drag
● Common associated symptoms:
- dementia,
- depression,
- urinary frequency,
- constipation,
- sleep disturbances
223
Would you describe the symptoms of Parkinson's disease as symmetrical or asymmetrical?
Asymmetrical = One side is always worse than the other
224
You ask a patient who you suspect to have Parkinson's disease to walk up and down the corridor to assess their gait, what features would be suggestive of PD?
Stooped posture
Asymmetrical arm swing
Small steps
Shuffling
225
Give 2 histopathological signs of Parkinson's disease
1. Loss of dopaminergic neurones in the substantia nigra
| 2. Lewy bodies
226
What investigations might you do in someone you suspect to have PD?
DaTscan
Functional neuroimaging - PET
Can confirm by reaction to levodopa
227
Describe the pharmacological treatment for Parkinson's disease
young onset + fit
- Dopamine agonist (ropinirole)
- MAO-B inhibitor (rasagiline)
- L-DOPA (co-careldopa)
frail + co-morbidities
- L-DOPA (co-careldopa)
- MAO-B inhibitor (rasagiline)
228
How does L-dopa work in the treatment of PD?
Precursor to dopamine and can cross the BBB (unlike dopamine)
- once in the brain it can be converted to dopamine
229
How do dopamine agonists work in the treatment of PD and give an example of one?
Reduced risk of dyskinesia
First line in patient <60
Ropinirole, pramipexole
230
How do MAO-B inhibitors work in the treatment of PD and give an example of one?
Inhibit MAO-B enzymes which breakdown dopamine -> increases amount of dopamine available
Rasagiline, selegiline
231
How do COMT inhibitors work in the treatment of PD and give an example of one?
Inhibit COMT enzymes which breakdown dopamine
| Entacapone, tolcapone
232
What surgical treatment methods are there for Parkinson's disease?
Deep brain stimulation of the sub-thalamic nucleus
| Surgical ablation of overactive basal ganglia circuits
233
Define Huntington's disease
Neurodegenerative disorder characterised by the lack of inhibitory neurotransmitter GABA - too much dopamine
autosomal dominant - 100% penetrance
234
Define chorea
Continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another
235
Describe the inheritance pattern seen in Huntington's disease
Autosomal dominant inheritance
| 100% penetrance
236
What triplet code is repeated in Huntington's disease?
CAG triplet repeat on chromosome 4
| >35 CAG = huntingtons
237
Briefly describe the pathophysiology of Huntington's disease
Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
238
Name the cardinal features of Huntington's disease
● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety
239
Name 3 signs of Huntington's disease
1. Abnormal eye movements
2. Dysarthria
3. Dysphagia
4. Rigidity
5. Ataxia
240
What investigations might you do in someone you suspect to have Huntington's disease?
● MRI/CT - loss of striatal volume
| ● Genetic testing
241
Describe the treatment of Huntington's disease
poor prognosis - no treatment
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis
242
What nerve is affected in carpal tunnel syndrome?
The median nerve (C6-T1)
243
what are the causes/risk factors of carpal tunnel syndrome
1. Pregnancy
2. Obesity
3. RA
4. DM
5. Hypothyroidism
6. Acromegaly
244
Describe the symptoms of carpal tunnel syndrome
- Intermittent and gradual onset
- Pins and needles, index and middle fingers
tend to be affected first
- Pain in thumb, index, middle and 1/2 ring fingers and palm, can reach
to the shoulder
- Numbness in same areas
- Weakness of same fingers, and loss of grip
- Worse at night, relieved by shaking
245
What investigations might you do in someone who you suspect to have carpal tunnel syndrome?
clinical diagnoses based on symptom presentation
EMG = slowing conduction velocity in median sensory nerves
Phalen's test = 1 min maximal wrist flexion --> symptoms
Tinel's test = tapping over nerve at wrist --> tingling
USS or MRI if other damage is suspected
246
What is the treatment for carpal tunnel syndrome?
- 1 in 4 cases will be self-limiting (usually 1 year)
- Pregnancy cases will resolve postpartum
- Rest the wrist, and try to avoid gripping/squeezing actions
- Splinting at night
- Local steroid injection
- Decompression surgery
247
What is autoimmune Guillain-Barre syndrome?
Acute inflammatory demyelinated ascending polyneuropathy affecting the PNS following an upper respiratory tract infection or GI infection
248
What can cause Guillain-Barre syndrome?
Bacteria
- Camplylobacter jejuni
- Mycoplasma
Viruses
- CMV
- EBV
- HIV
- Herpes zoster
249
Describe the pathophysiology of Guillain-Barre syndrome
Same antigens on infectious organisms as Schwann cells (PNS) --> autoantibody mediated nerve cell damage -> via molecular mimicry
Schwann cell damage consists of demyelination, which results in a reduction in peripheral nerve conduction --> causes acute polyneuropathy
spreads from proximal to distal
250
what are the clinical features of Guillain-Barre syndrome
```
Breathing problems
Back pain
Sensory disturbance
Sweating
Urinary retention
```
1. Ascending symmetrical muscle weakness 1-3 weeks post-infection (proximal muscles most affected - trunk, respiratory, CN) TOES TO NOSE WEAKNESS
2. Pain in legs, back is rare
3. sensory loss in lower extremities
4. Reflexes lost early on (LMN sign)
5. Autonomic features =
- reduced sweating
- reduced heat tolerance
- paralytic ileus - intestinal obstruction w/o blockage
- urinary hesitancy
251
What investigations might you do in someone you suspect has Guillain-Barre syndrome?
- Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
- Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
- bloods - FBC, U&E, LFT, TFT
- Spirometry = respiratory involvement
- ECG
252
Describe the treatment for Guillain-Barre syndrome
- If FVC <1.5L/80% = ventilate and ITU monitoring
- IV immunoglobulin (IvIg) for 5 days = decrease duration and severity of paralysis
- Plasma exchange
- Low molecular weight heparin (LMWH) - SC ENOXAPARIN
- Analgesia
253
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?
If a patient has IgA deficiency - can cause severe allergic reaction
254
Define stroke
Rapid onset of neurological deficit due to a vascular lesion lasting >24 hours and associated with infarction of central nervous tissue
poor blood flow to the brain causes cell death
255
How can strokes be classified?
1. Ischaemic (85%) - blood clot in the blood vessel to the brain
2. Haemorrhagic (15%) - bleed in small blood vessel in/around brain
256
What are the causes of an ischaemic stroke?
- small vessel occlusion by thrombus
- atherothromboembolism (e.g. from carotid artery)
- cardioembolism (post MI, valve disease, IE)
- hyper viscosity
- hypoperfusion
- vasculitis
- fat emboli from a long bone fracture
- venous sinus thrombosis
257
What are the causes of an haemorrhagic stroke
Bleeding from the brain vasculature
1. Hypertension - stiff and brittle vessels, prone to rupture
2. Secondary to ischaemic stroke - bleeding after reperfusion
3. Head trauma
4. Arteriovenous malformations
5. Vasculitis
6. Vascular tumours
6. Carotid artery dissection
258
what are the risk factors for ischaemic stroke?
1. Age
2. Male
3. Hypertension
4. Smoking
5. Diabetes
6. Recent/past TIA
7. Heart disease - IHD, AF, valve disease
8. Combined oral contraceptive
259
Give 3 signs of an ACA stroke
1. Leg weakness - contralateral
2. Sensory disturbance in legs
3. Gait apraxia
4. Incontinence
5. Drowsiness
6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
7. truncal ataxia - can't sit or stand unsupported
260
Give 3 signs of a MCA stroke
1. Contralateral arm and leg weakness and sensory loss
2. Hemianopia
3. Aphasia
4. Dysphasia
5. Facial droop
261
Give 3 signs of a PCA stroke
visual issues
1. Contralateral homonymous hemianopia
2. Cortical blindness
3. Visual agonisa
4. Prosopagnoisa
5. Dyslexia
6. Unilateral headache
262
What is visual agnosia?
An inability to recognise or interpret visual information
263
What is prosopagnosia?
Inability to recognise a familiar face
264
A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?
Middle cerebral artery
265
A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?
Anterior cerebral artery
266
A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?
Posterior cerebral artery
267
Give 3 differential diagnosis's for a stroke
1. Hypoglycaemia
2. Intracranial tumour
3. Head injury +/- haemorrhage
268
What investigation could you do to determine whether someone has had a haemorrhagic or ischaemic stroke?
Head CT scan (before treatment)
269
What is the treatment for an ischaemic stroke?
Immediate management:
- CT/MRI to exclude haemorrhagic stroke
- aspirin 300mg
Antiplatelet therapy
- aspirin 300mg for 2 weeks
- clopidogrel daily long term
Anticoagulation (e.g. warfarin) for AF
thrombolysis
- within 4.5 hrs of onset
- IV alteplase
- lots of contraindications (can cause massive bleeds)
mechanical thromboectomy
- endovascular removal of thrombus
270
How does alteplase work?
Converts plasminogen --> plasmin
| So promotes breakdown of fibrin clot
271
When can you do thrombolysis in someone with an ischaemic stroke?
Up to 4.5. hours post onset of symptoms
272
What is primary prevention of strokes?
Risk factor modifcaiton
- Antihypertensives for HTN
- Statins for hyperlipiaemia
- Smoking cessation
- Control DM
- AF treatment = warfarin/NOAC's
273
What is secondary prevention of strokes?
2 weeks of aspirin --> long term clopidogrel
274
What non-pharmacological treatment options are there for people after a stroke?
1. Specialised stroke units
2. Swallowing and feeding help
3. Phsyio and OT
4. Neurorehab - physio + speech therapy
275
What is a TIA?
sudden onset, brief episode of neurological deficit due to temporary, focal cerebral ischaemia
symptoms are maximal at onset and lasts 5-15 mins (<24hrs)
276
Give 3 causes of a TIA
1. Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
2. Cardioembolism - in AF, after MI, valve disease/prosthetic valve
3. Hyperviscosity - polycythaemia, sickle cell, high WBCC
4. hypoperfusion - postural hypotension, decreased flow
277
Describe the pathophysiology of a TIA
Cerebral ischaemia due to lack of O2 and nutrients --> cerebral dysfunction without infarction (no irreversible cell death)
symptoms are maximal at onset -> usually last 5-15 mine (<24hrs)
278
what are the signs of a carotid TIA?
1. Amaurosis fugax = retinal artery occlusion --> vision loss
2. Aphasia
3. Hemiparesis
4. Hemisensory loss
5. hemianopia
279
what are the signs of a vertebrobasilar TIA?
1. Diplopia, vertigo, vomiting
2. Choking and dysarthria
3. Ataxia
4. Hemisensory loss
5. Hemianopic/bilateral visual loss
6. tetraparesis
7. loss of consciousness
280
what are the differential diagnosis's for a TIA
1. Migraine aura
2. Epilepsy
3. Hypoglycaemia
4. Hyperventilation
5. retinal bleed
6. syncope - due to arrhythmia
281
What investigations would you do in someone who you suspect to have a TIA?
first line = diffusion weighted MRI or CT
second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found)
Bloods
- FBC - look for polycythaemia
- ESR - raised in vasculitis
- U&Es, glucose
ECG
echocardiogram
282
What is it essential to do in someone who has had a TIA?
Assess their risk of having stroke in the next 7 days = ABCD2 score
283
What is the ABCD2 score?
Assesses risk of stoke in the next 7 days for those who have had a TIA
- age
- BP
- clinical features - unilateral weakness, speech disturbance
- duration of TIA
- presence of diabetes mellitus
284
What classifies as a high risk stroke patient?
- have ABCD2 score >4
- have AF
- >1 TIA in a week
285
Within how long should someone with a suspected TIA been seen by a specialist?
Within 7 days
286
What is the treatment for a TIA?
immediate treatment = aspirin 300mg and refer to specialist within 24hrs
control CV risk factors
- BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
- smoking cessation
- statin - SIMVASTATIN
- no driving for 1 month
antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily
anticoagulation (e.g. WARFARIN) for patients with AF
carotid endarterectomy
- if >70% carotid stenosis
- reduces stroke/TIA risk by 75%
287
Give 3 causes of spinal cord compression
- trauma,
- tumours - most common spinal metastases are
breast, prostate and lung cancer
- central disc protrusion,
- prolapsed disc (L4-5 and L5-S1 most common),
- epidural haematoma,
- infection,
- cervical spondylitic myelopathy
288
Give 3 signs and symptoms of spinal cord compression
```
Red flag signs:
- Loss of bladder or bowel function,
- UMN signs in the lower limbs (e.g. clonus, hyperreflexia),
- LMN signs in the upper
limbs (e.g. atrophy)
```
● Symptoms depend on the injury type and site
- Can include paraplegia,
- pain,
- paraesthesia,
- changes to tendon reflexes
289
What investigations might you do in someone with suspected spinal cord compression?
Urgent MRI/CT scan
● X-ray whole spine
● MRI if indicated
● Renal function
● Haemoglobin - monitor blood loss
290
What is the treatment for spinal cord compression?
● Acute spinal cord compression is a neurosurgical emergency
● Dexamethasone until treatment plan confirmed
● Catheterisation
● Analgesia
● Surgical decompression if indicated
● Chemotherapy if indicated
291
Briefly describe the pathophysiology of cauda equina syndrome
Spinal compression at or caudal to L1 --> disrupts sensation and movement - flaccid and areflexic weakness
292
Give 3 causes of cauda equina syndrome
1. Lumbar disc herniation at L4/5 or L5/S1
2. Tumour
3. Trauma
4. Infection
5. late-stage ankylosing spondylitis
6. post-operative haematoma
7. sarcoidosis
293
what are the clinical features of cauda equina syndrome
```
● Sudden onset - hours
● Saddle paraesthesia
● bilateral sciatica
● Bladder/bowel dysfunction
● erectile dysfunction
● Motor problems
● Lower back pain
● Bilateral LMN weakness, absent ankle reflex (flaccid and areflexic)
```
294
What investigations might you do to see if someone has cauda equina syndrome?
● Medical emergency
- immediate referral
● Rectal exam - loss of anal tone/sensation
● MRI spine
● knee flexion (L5-S1) and ankle plantar flexion (S1-S2)
295
How do you treat cauda equina syndrome?
```
● Surgical decompression is essential
● Immobilise spine
● Anti-inflammatory agents
● Antibiotics if infection present
● Chemotherapy if indicated
```
* Microdiscectomy - removal of part of the disc - may tear dura!
* Epidural steroid injection - more effective for leg pain
* Surgical spine fixation - if vertebra slipped
* Spinal fusion - reduces pain from motion and nerve root inflammation
296
What is treatment for sciatica without neurological signs?
Conservative management - physio and NSAIDs
297
Define spondyloisthesis
Slippage of vertebra over the one below
298
Define spondylosis
Degenerative disc disease
299
What are the 4 stages of a seizure?
1. Prodromal - often emotional signs
2. Aura
3. Ictal
4. Post-ictal - often drowsy and confused
300
Give 3 activities that can trigger trigeminal neuralgia
1. Washing your face
2. Eating
3. Shaving
4. Talking
301
How long do you wait for before doing a lumbar puncture in someone with a suspected subarachnoid haemorrhage?
At least 12 hours
You need to wait or the Hb to break down and then CSF will become yellow - sign that there is a bleeding in subarachnoid space (xanthochromia)
302
what are the investigations for alzheimer's disease?
● MMSE
● Bloods - TFTs, B12 (check for other causes)
● Memory clinic assessment
● MRI
303
what is the treatment for alzheimer's disease?
No cure
● Supportive therapy, e.g. carers, changes to the home, help with daily activities
● Medication to manage symptoms
○ Acetylcholinesterase (AChE) inhibitors, e.g. rivastigmine, galantamine, memantine
304
what is the epidemiology of Alzheimer's disease?
Most common type of dementia
| ● Mainly affects those over 65
305
what are the risk factors for Alzheimer's disease?
- Down’s syndrome,
- ApoE E4 allele homozygosity,
- reduced cognitive activity,
- depression/loneliness
306
what is the epidemiology of frontotemporal dementia?
● Progressive dementia
| ● More common dementia in those under 65, but still only 5% of dementias
307
what is the pathophysiology of frontotemporal dementia?
● Atrophy of the frontal and temporal lobes
● Loss of neurons, but no plaque formation
● Tau +ve or TDP-43 +ve inclusions
308
what are the risk factors for frontotemporal dementia?
50% dominant inheritance
309
what are the investigations for frontotemporal dementia?
Bloods - B12, TFTs, U&Es (?other causes)
● FBC and LFTs for suspected encephalopathy
● MMSE
● MRI - frontal/temporal atrophy
310
what is the treatment for frontotemporal dementia?
● No cure
● Supportive therapy, e.g. carers, help setting up a stable routine, home changes for motor difficulties, speech and language therapy
● SSRIs - help with behaviour symptoms
● Levodopa/carbidopa if Parkinson’s symptoms present
● Stopping exacerbating drugs
311
what is the epidemiology of vascular dementia?
● Second most common dementia, globally
○ 17% of dementia in the UK
● Result of multiple, small infarcts
312
what are the risk factors for vascular dementia?
```
smoking,
history of TIAs,
AF,
hypertension,
DMT1,
hyperlipidaemia,
obesity,
coronary heart disease
```
313
what is the pathophysiology of vascular dementia?
is based on the location and size of the original infarct, and number and location of consequent infarcts
● A single stroke double the risk of developing vascular dementia
314
what are the investigations for vascular dementia?
● Full history important - previous stroke/TIA?
● Cognitive impairment screen
○ Orientation, attention, language function,
visuospatial functions, motor control
● Medication review - ?other cause
● MRI - looking for previous infarcts
315
what is the treatment for vascular dementia?
● Supportive therapy, e.g. carers, home changes,
routine help, cognitive simulation programmes
● No pharmacological treatment for the dementia
itself
● SSRIs or anti-psychotics to control symptoms,
e.g. lorazepam
● Prognosis is 3-5 years from diagnosis
316
what are the investigations for Lewy Body dementia?
● MMSE or 6-item cognitive impairment test (6-CIT)
● Bloods - B12, TFTs, U&E, MRI (?other cause)
● MSU to check for urine infection
317
what is the diagnostic criteria for Lewy Body dementia?
○ Presence of dementia with 2 of:
- fluctuating attention and concentration,
- recurrent well-formed visual hallucinations,
- spontaneous Parkinsonism
○ If there is only 1 of the 3 core features, diagnosis can also be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia
318
what is the treatment for Lewy Body dementia?
● Refer to a specialist
● Supportive therapy - cognitive stimulation, exercise programmes, at-home care
● Cholinesterase inhibitors, e.g. rivastigmine suggested to treat cognitive decline
● Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe
sensitivity reactions
319
what is the epidemiology of Parkinson's disease?
Second most common neurodegenerative disorder (after Alzheimer’s)
Typically develops between 55-65 years of age
320
what are the other causes of Parkinson's disease?
- Drug induced Parkinsonism - caused by dopamine
antagonists, e.g. clozepine
- encephalitis
- exposure to certain toxins, e.g. manganese dust
321
what is the 3 step diagnostic pathway for diagnosing Parkinson's disease?
1) Diagnosis of Parkinsonian syndrome
○ Bradykinesia (required) plus one of rigidity, resting tremor, or postural instability
2) Exclusion criteria (none to be met)
○ History of stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, babinski’s sign, early severe dementia, negative response to large L-dopa dose
3) Supportive criteria (3 or more required)
○ Unilateral onset, rest tremor present, progressive, excellent response to L-dope (70-100%), visual hallucinations
322
what is foot drop?
Difficulty in lifting the front part of the foot,
resulting in dragging of the toes
● Can be permanent or temporary
323
Damage to which nerve causes foot drop?
Caused by damage to the common peroneal nerve - L4-S1 (also called common fibular
nerve)
324
what are the causes of foot drop?
```
injury,
lower back damage,
tumour,
hip replacement,
cauda equina syndrome,
multiple sclerosis
```
325
what are the clinical features of foot drop?
```
● Unilateral symptoms
● Complaint of one foot dragging across the
floor when walking
● Tripping
● Numbness in the same side
● Weakness in the same side
```
326
what are the investigations for foot drop?
● Foot drop itself can be a clinical diagnosis
● Need to find the underlying cause:
○ X-ray, USS, CT, MRI
○ Nerve conduction study
327
what is the treatment for foot drop?
```
● Brace or splint
● Physiotherapy
● Specialised shoes - prevent foot drop when walking
● Nerve stimulation
● Surgery if indicated
```
328
what is the epidemiology of TIA?
- 15% of strokes are preceded by TIA
- can foreshadow MI
- male > female
- more common in black people (predisposition to hypertension and atherosclerosis)
329
what are the risk factors for TIA?
- age
- hypertension
- smoking
- diabetes
- heart disease - AF
- combined oral contraceptive pill
- hyperlipidaemia
- peripheral artery disease
- clotting disorder
- vasculitis
330
what are the differential diagnoses for TIA?
```
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis
Syncope - E.g. due to an arrythmia
Retinal bleed
```
331
what percentage of TIAs are found in the carotid territory?
```
90% = carotid territory
10% = vertebrobasilar territory
```
332
what is the pathophysiology of an ischaemic stroke?
- arterial disease and atherosclerosis is the main pathological process
- thrombosis occurs at the site of atheromatous plaque in carotid/vertebral/cerebral arteries
- Emboli arise from atheromatous plaques in the carotid/vertebrobasilar arteries or from the left atrium in atrial fibrillation
- Cardiac artery stenosis, hypoperfusion
333
what is the pathophysiology of haemorrhagic stroke?
bleeds caused by trauma, aneurysm rupture, thrombolysis, carotid artery dissection
334
what are lacunar infarcts (ischaemic stroke)?
- Small infarcts
- From occlusion of a single small perforating artery supplying a subcortical area
- Can happen in:
- Internal capsule
- Basal ganglia
- Thalamus
- Pons
335
what is the clinical presentation of lacunar infarcts (ischaemic stroke)?
Depends on the area affected
One of:
- Sensory loss
- Weakness (unilateral)
- Ataxic hemiparesis
- Dysarthria
- Motor speech problems
336
which areas of the brain can be affected by lacunar infarcts (ischaemic stroke)?
Internal capsule
Basal ganglia
Thalamus
Pons
337
what is the clinical presentation of brainstem infarcts (ischaemic stroke)?
- Quadriplegia
- Facial numbness & paralysis
- Gaze & vision disturbances
- Dysarthria & speech impairment
- Vertigo, nausea, vomiting
- Cerebellar signs
- Palatal paralysis & diminished gag reflex
- Altered consciousness
- Locked-in syndrome
- Coma
338
what are the investigations for ischaemic stroke?
- urgent head CT before treatment
- shows site
- pulse, BP and ECG
- look for AF and MI
- bloods
- FBC - look for polycythaemia
- glucose - rule out hypoglycaemia
- ESR - raised in vasculitis
- cholesterol
- INR - if on warfarin
- U&Es
- MRI
- more sensitive but may be negative in first few hours after infarct
- indicated if diagnosis is uncertain
339
what are the different types of haemorrhagic stroke?
- intracerebral haemorrhage
| - subarachnoid haemorrhage
340
what are the contraindications of thrombolysis (IV alteplase)?
- Recent surgery last 3 months
- Recent arterial puncture
- History of active malignancy (highly vascular thus increased
bleeding risk)
- Evidence of brain aneurysm
- Patient on anticoagulation
- Severe liver disease (abnormal clotting)
- Acute pancreatitis
- Clotting disorder
341
what is the treatment for haemorrhagic stroke?
- frequent GCS monitoring
- anticoagulants are contraindicated (any anticoagulants should be reversed with vitamin K)
- control hypertension
- decompression of raised ICP - MANNITOL
- surgery may be required
342
what is an intracerebral haemorrhage?
- Sudden bleeding into brain tissue
- Due to rupture of a blood vessel within the brain
- Like an ischaemic stroke, this leads to infarction, due to O2 deprivation
- Pooling blood increases intracranial pressure (ICP)
- ~10% of strokes
- Higher mortality: up to 50%
343
what are the major risk factors for intracerebral haemorrhage?
```
Hypertension
Age
Alcohol
Smoking
Diabetes
```
Anticoagulation
Thrombolysis
344
what are the causes of intracerebral haemorrhages?
- Hypertension
- Stiff & brittle vessels, prone to rupture
- Microaneurysms
- Secondary to ischaemic stroke
- Bleeding after reperfusion
- Head trauma
- Arteriovenous malformations
- Vasculitis
- Vascular tumours
- Brain tumours
- Cerebral amyloid angiopathy
- Carotid artery dissection
345
what is the pathophysiology of intracerebral haemorrhage?
1. Increased ICP puts pressure on skull, brain & blood vessels - healthy tissue can die
2. CSF obstruction - hydrocephalus
3. Midline shift
4. Tentorial herniation
5. Coning - compression of
brainstem
346
what is the clinical presentation of intracerebral haemorrhage?
similar to ischaemic stroke
pointers to haemorrhage:
- sudden loss of consciousness
- severe headache
- meningism
- coma
347
what are the investigations for intracerebral haemorrhage?
- same as ischaemic stroke
| - CT/MRI is essential
348
what is the management for intracerebral haemorrhage?
- stop anticoagulants immediately
- effects reversed with clotting factor replacement
- control of BP - IV drugs
- reduce ICP
- mechanical ventilation
- IV mannitol
- refer for neurosurgical intervention if:
- hydrocephalus
- coma
- brainstem compression
349
what are the differential diagnoses for subarachnoid haemorrhages?
- headache - migraine, cluster headache
- meningitis
- intracerebral haemorrhage
- cortical vein thrombosis
- carotid/vertebral artery dissection
350
what is a subarachnoid haemorrhage?
Spontaneous bleeding into subarachnoid space
Space between arachnoid mater & pia mater
Can be catastrophic
351
what is a subdural haematoma?
- Bleeding into subdural space - space between dura mater & arachnoid mater
- Due to rupture of a bridging vein - run from cortex to venous sinuses. They are vulnerable to deceleration injury
- Usually due to head trauma
- Other causes include dural metastases
- Massive latent interval – weeks to months
- Very treatable
352
what are migraines?
recurrent throbbing headache often preceded by an aura & associated with nausea, vomiting and visual changes
353
what is the epidemiology of migraines?
Most common causes of episodic headache ie. Recurrent
More common in females (roughly 3x)
90% have onset before 40yrs
354
what are the risks for migraines?
- genetics - family history
- female
- age - majority of first migraines are in adolescence
355
what are the investigations for migraines?
- usually made with little/no investigations, however if there are red flags further investigation is required
- always examine eyes, BP, head and neck (muscles, scalp, temporal arteries)
- lab tests e.g. CRP, ESR
- CT/MRI
- LUMBAR PUNCTURE
356
what are the red flag indications for CT/MRI in migraines?
- worst/severe headache i.e. "thunderclap"
- change in pattern of migraine
- abnormal neurological exam
- onset > 50yrs
- epilepsy
- posteriorly located headache
357
what are the red flag indications for a lumbar puncture in migraines?
- thunderclap headache
| - severe, rapid onset headache / progressive headache / unresponsive headache
358
when are triptans contraindicated?
in ischaemic heart disease, coronary spasm and uncontrolled high BP
family history of CVD, stroke, DM and high cholesterol
359
what are the side effects of triptans?
- arrhythmias
- angina +/- MI
- recurrence of migraines - higher frequency
360
what preventative measures can be taken for migraines?
- beta blockers e.g. propranolol
- TCAs e.g. amitriptyline
- anticonvulsant e.g. topiramate
- acupuncture
361
when should preventative measures be taken for migraines?
- if >2 attacks per month
| - require acute meds >2x per week
362
what is a cluster headache?
Episodic headaches lasting from 7 days up to 1 year (although usually 2-3wks) with pain-free periods in between that last ~4wks
363
what is the epidemiology of cluster headache?
Considered the most disabling of primary headaches
Much rarer than migraines, and more common in males (~4x)
Typically affects adults with onset usually 20-40yrs
364
what are the risk factors of cluster headaches?
Smoker
Alcohol
Male
Genetics - autosomal dominant gene has a link
365
what are the preventative measures for cluster headaches?
- 1st line = verapamil (CCB)
- prednisolone
- reduce alcohol consumption and stop smoking
366
what are the investigations for cluster headaches?
- diagnosed by clinical examination
| - at least 5 attacks fulfilling the presentation criteria
367
what are the triggers for tension headaches?
- stress
- sleep deprivation
- bad posture
- hunger
- eyestrain
- anxiety
- noise
368
what is the clinical presentation of tension headache?
usually one of the following:
- bilateral
- pressing/tight and non-pulsatile (like an elastic band)
- mild/moderate intensity
- +/- scalp tenderness
no aura, vomiting or sensitivity to head movement
can be some pressure behind the eyes, but pain isn't localised to be around the eye
369
which medications commonly cause medication-overuse headaches?
- worsens whilst on regular analgesia, especially opioids
| - mixed analgesics e.g. paracetamol + codeine/opiates, ergotamine and triptans
370
why are lumbar punctures contraindicated in brain tumours?
withdrawing CSF may provoke immediate coning
371
which is more common out of primary and secondary brain tumours?
secondary brain tumours are 10 times more common
372
what is wernicke's encephalopathy caused by?
depletion of thiamine (vitamin B1)
373
what is the clinical presentation of wernicke's encephalopathy?
- classic triad
- confusion
- ataxia
- ophthalmoplegia
- sign
- asterixis (liver flap) - general sign of metabolic encephalopathy
374
what diseases does wernicke's encephalopathy occur in?
- chronic alcoholism
- severe starvation
- prolonged vomiting
375
what are the investigations for wernicke's encephalopathy?
- diagnosed via clinical examination
376
what is the management for wernicke's encephalopathy?
- pabrinex - IV B-vitamins (including thiamine)
377
what are the complications of wernicke's encephalopathy?
if not managed appropriately
- fatal in 20%
- can progress to korsakoff's syndrome
378
what is korsakoff's syndrome?
- irreversible
- long term brain damage due to vitamin B1 deficiency
- symptoms = decreased ability to acquire new memories, retrograde amnesia, confabulation (invented memories)
379
what are the causes and risk factors of MND?
- usually sporadic and unknown cause
| - 5-10% are familial = SOD-1 mutation
380
what is the pathophysiology of MND?
- degenerative condition affecting anterior horn motor neurone cells in the brain and the spinal cord
- damage is caused by oxygen species which damage DNA,, lipids and proteins
- causes both UMN and LMN dysfunction
- there is no sensory loss or sphincter disturbance
- it never affects eye movements
381
what are the 4 different types of MND? do they affect LMN or UMN?
amyotrophic lateral sclerosis (ALS) - UMN + LMN
progressive muscular atrophy (PMA) - LMN only
progressive bulbar palsy (PBP) LMN only
primary lateral sclerosis (PLS) UMN only
382
what is the epidemiology of ALS (MND)?
- most common form of MND (50%)
- some familiar inheritance - SOD1 and C90RF72 genes
- common ages of onset 40-50 (familial) and 58-63 (sporadic)
383
what is the clinical presentation of ALS?
● Presents with signs of degeneration of upper and
lower motor neurons
● progressive paralysis and eventual respiratory failure
● Asymmetric onset
● Babinski sign +ve
● Fasciculations of the tongue
● Any corticobulbar signs indicate a worse prognosis:
○ Brisk jaw reflex
○ Dysarthria (difficulty speaking)
○ Dysphagia (difficulty swallowing)
○ Sialorrhoea (excess salivation)
384
what are the clinical features of progressive bulbar palsy (PBP) in MND?
CN 9-12
- LMN in the brain stem
- pharyngeal muscle weakness
- progressive loss of speech (hoarse, quiet, nasal)
- tongue atrophy (flaccid)
385
what are the clinical features of primary lateral sclerosis (PLS) in MND?
- UMN of the arm, legs and face
- movements become slow
- progressive tetraparesis
386
what are the clinical features of progressive muscular atrophy (PMA) in MND?
- LMNs only
- muscle wasting
- clumsy hand movements
- fasciculations
- muscle cramps
387
what are the risk factors for Guillain-Barre syndrome (GBS)?
- history of respiratory or GI infection 1-3 weeks prior to onset
- vaccinations have been implicated
- post-pregnancy
388
what is the epidemiology of Guillain-Barre syndrome?
● Increased incidence in males
| ● Peak ages are 15-35, and 50-75
389
what are the side effects of pyridostigmine used to treat myasthenia gravis?
- increased salivation
- lacrimation
- sweats
- vomiting
- miosis (excessive pupillary constriction)
- diarrhoea
390
what is myasthenic crisis?
a complication of myasthenia gravis
weakness of the respiratory muscles during a relapse can be life-threatening
391
what is the treatment for myasthenic crisis?
- monitor FVC
- plasmapheresis and IV immunoglobulin
- identify and treat trigger of relapse e.g. infection, medications
392
where are MS demyelination plaques commonly found?
- optic nerves
- around ventricles of the brain
- brainstem and cerebellar connections
- corpus callosum
- cervical cord (corticospinal tract and dorsal columns)
393
what is relapsing and remitting MS?
* MOST COMMON PATTERN of MS
* Symptoms occur in attacks (relapses) with onset over days and typically recovery, either partial or complete, over weeks
* Periods of good health or remission are followed by sudden symptoms or relapses
* Patients may accumulate disability over time if they do not recover fully after relapses
394
what is secondary progressive MS?
• Follows on from relapsing & remitting MS
• Late stage of MS that consists of gradually worsening symptoms with
fewer remissions
• 75% of patients with relapsing-remitting MS will eventually evolve into a secondary progressive MS by 35yrs after onset
395
what is primary progressive MS?
• Gradually worsening disability WITHOUT relapses or remissions
• Typically presents later and is associated with fewer inflammatory
changes on MRI
396
what is the classic presentation of MS in exams?
○ A female 20-40 years old
○ Any 2 of the symptoms of MS
○ Optic neuritis is often shown as first symptom - disseminate in space!
397
what are the investigations for herpes zoster?
- clinical diagnosis
| - eruption of rash is virtually diagnostic
398
what are the risk factors of herpes zoster?
- increasing age
- immunocompromised
- HIV, hodgkin's lymphoma and bone marrow transplants
399
what is the epidemiology of herpes zoster?
- 90% of children have been exposed to chicken pox before 16 years
- can affect all ages - more seen in elderly
- incidence and severity increases with age
400
what is the pathophysiology of herpes zoster?
- viral infection affecting peripheral nerves
- when latent virus is reactivated in the dorsal root ganglia it travels down the affected nerve via sensory root in dermatomal distribution over 3-4 days
- results in perineural and intramural inflammation
401
what is post-herpetic neuralgia?
- pain lasting for more than 4 months after developing shingles
- occurs in 10% of patients - often elderly
- burning, intractable pain
- responds poorly to analgesics
402
what is the treatment for post-herpetic neuralgia?
- tricyclic antidepressant - AMITRIPTYLINE
- anti-epileptic - GABAPENTIN
- anti-convulsant - CARBAMEZAPINE
403
what is sciatica?
- pain numbness and tingling sensation
| - radiates from lower back and travels down one of the legs to the foot and toes
404
what are the lumbar puncture results for meningitis caused by bacteria?
- cells = polymorphs
- proteins = raised
- glucose = low
- CSF = turbid colour
405
what are the lumbar puncture results for meningitis caused by TB?
- cells = lymphocytes
- proteins = raised
- glucose = normal/low
406
what are the lumbar puncture results for meningitis caused by viruses?
- cells = lymphocytes
- proteins = normal
- glucose = normal
407
what antibiotic is used in meningitis if S. Pneumoniae is suspected?
vancomycin
408
what antibiotic is used in meningitis if listeria is suspected?
ampicillin (or amoxicillin) and gentamycin
409
what is the treatment for viral meningitis?
no specific treatment
analgesia
antipyretics
hydration
410
what are the risk factors for meningitis?
- immunosuppression
- elderly
- pregnant
- crowding (university)
- diabetes
- malignancy
- IV drug use
- sickle cell anaemia
- adrenal insufficiency
411
what is the pathophysiology of meningitis?
- Microorganisms reach the meninges from the ears,
nasopharynx, cranial injury or congenital meningeal defect or by bloodstream spread
- Acute bacterial meningitis:
• Typically sudden
• The pia-arachnoid is congested with polymorphs
• A layer of pus forms which may organise to form adhesions causing
cranial nerve palsies and hydrocephalus
- Chronic infection e.g. TB:
• Brain is covered in a viscous grey-green exudate with numerous
meningeal tubercles
- Viral meningitis:
• Predominantly lymphocytic inflammatory CSF reaction WITHOUT PUS FORMATION
• no cerebral oedema
412
what is meningococcal septicaemia?
- When bacteria invades into blood
- Presence of endotoxin in bacteria leads to a inflammatory cascade
- Petechial rash + signs of sepsis = meningococcal septicaemia
413
what is the cardinal sign of meningococcal septicaemia?
Petechial rash + signs of sepsis = meningococcal septicaemia
414
what are the risk factors for epilepsy?
FHx
Premature babies, especially if they are small for their gestational age
Abnormal cerebral blood vessels
Drugs eg. cocaine
415
what is the prodrome element of a seizure?
- Precedes the seizures, usually by hours/days
| - Weird feeling eg. mood/behaviour changes
416
what is the post-ictal element of a seizure?
- The period after a seizures
- Headache, confusion, myalgia, sore tongue (often bitten)
- Temporary weakness after focal seizure in motor cortex = Post-Ictal Todd’s palsy
- Dysphasia following temporal lobe seizure
417
what are primary/generalised seizures?
- Simultaneous electrical discharge throughout the whole cortex, with no features that suggest localisation to only one hemisphere/lobe
- Bilateral and symmetrical motor manifestations
- ALWAYS ASSOCIATED WITH LOSS OF CONSCIOUSNESS & LACK OF AWARENESS
418
what are focal (partial) seizures?
- Focal onset with features that can be referrable to a single lobe eg. temporal lobe
- Often seen with underlying structural disease ie. There is an underlying cause
- Electrical discharge is limited to one lobe, in one hemisphere
- These may later progress to become generalized seizures
419
what are tonic seizures?
```
High tone (hence the name) = rigid, stiff limbs
Will fall to floor if standing due to stiff limbs
```
420
what are clonic seizures?
Rhythmic muscle jerking (ie. Clonus, the UMN sign)
421
what are tonic-clonic seizures (grand mal)?
As the name suggests a combination of tonic & clonic seizures
This is your stereotypical “Shaking” seizures due to the mix of on/off rigidity & muscle jerking
422
what is a myotonic seizure?
Isolated jerking of a limb/face/trunk
| “disobedient limb” or “thrown to the floor”
423
what is an atonic seizure?
Complete opposite to tonic seizure, loss of muscle tone = floppy
424
what is an absence (petit mal) seizure?
Common in childhood but usually goes by adulthood, however there is an increased risk of developing generalized tonic-clonic seizures as an adult
Will go pale and ”stare blankly” for a few seconds
Often suddenly stop talking mid-sentence & do not realise they have had an attack
425
what are simple focal (partial) seizures?
- No affect on consciousness or memory
- Awareness unimpaired but will have focal motor, sensory, autonomic or psychic symptoms depending on the affected lobe
- No post-ictal symptoms
426
what are complex focal (partial) seizures?
Memory/awareness is affected before, during or immediately after the seizure
Most commonly arises from the temporal lobe > affects speech, memory & emotion
Post-ictal confusion is common if temporal lobe, whereas recovery is often swift if the frontal lobe is affected
427
what are the characteristics of temporal lobe specific seizures?
Aura (80%); deja-vu, auditory hallucinations, funny smells, fear
- Anxiety, out-of-body experiences
- Automatisms eg. lip smacking
428
what are the characteristics of frontal lobe specific seizures?
Motor features eg. posturing, peddling movements of leg
JACKSONIAN MARCH – seizures march up/down the motor homunculus
Post-Ictal Todd’s palsy
Starts distally in a limb & works its way upwards to the face
429
what are the characteristics of parietal lobe specific seizures?
Sensory disturbances eg. tingling/numbness
430
what are the characteristics of occipital lobe specific seizures?
Visual phenomena eg. spots, lines, flashes
431
what is a partial seizure with secondary generalization?
2/3 patients with partial seizures will develop generalized seizures, usually generalized tonic-clonic
These start focally & spread widely throughout the cortex
432
what are the characteristics of non-epileptic seizures?
Non-epileptic seizures are entirely situational
Eg. metabolic disturbances; low Na+, hypoxia
Can be related to syncope
Non-epileptic seizures are typically longer with closed eyes & mouth
Non-epileptic do not occur during sleep and do not involve incontinence or tongue-biting
There are pre-ictal anxiety symptoms in non-epileptic eg. they know they are about to happen
433
what clinical signs indicate a diagnosis of epilepsy rather than syncope?
```
Tongue-biting
Head turning
Muscle pain
LOC
Cyanosis
Post-ictal symptoms
```
434
what are the investigations for epilepsy
Electroencephalogram (EEG) = supports diagnosis
MRI/ CT head = rule out space-occupying lesions
Bloods
FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose = rule out metabolic disturbances
Genetic testing
If suspected genetic cause -> juvenile myoclonic epilepsy
435
what is the emergency treatment for epilepsy?
- ABCDE
- check glucose
- RECTAL/IV DIAZEPAM or LORAZEPAM
- IV PHENYTOIN loading
- mechanical ventilation
436
what is the treatment for generalised tonic-clonic epilepsy?
Sodium Valproate for Males & women unable to childbear,
Lamotrigine to females of childbearing potential
437
what is the treatment for generalised tonic/atonic epilepsy?
Sodium Valproate for Males & women unable to childbear,
Lamotrigine to females of childbearing potential
438
what is the treatment for generalised myoclonic epilepsy?
Sodium Valproate for Males & women unable to childbear,
Levetiracetam/Topiramate to females of childbearing potential
439
what is the treatment for absence (petit mal) epilepsy?
Sodium Valproate for Males & women unable to childbear,
Ethosuximide to females of childbearing potential
440
what are the side effects of sodium valproate?
- weight gain
- hair loss
- liver failure
441
why is sodium valproate not prescribed to women during pregnancy?
it is teratogenic
442
what are the side effects of lamotrigine?
maculopapular rash
blurred vision
vomiting
443
what are the side effects of carbamazepine?
```
diplopia
rashes
leucopenia
impaired balance
drowsiness
```
444
what are the side effects of ethosuximide?
rashes
| night terrors
445
what is status epilepticus?
- medical emergency
| - continuous seizures for over 5 minutes without recovery of consciousness
446
what is trigeminal neuralgia?
described as a chronic, debilitating condition resulting in
| intense and extreme episodes of pain
447
what are the risk factors for trigeminal neuralgia?
- Hypertension is the main risk factor
- Triggers:
• Washing affected area,
shaving,
eating,
talking
dental prostheses
448
what is the clinical presentation of trigeminal neuralgia?
- ALMOST ALWAYS UNILATERAL
- At least 3 attacks of unilateral facial pain
- Facial pain occurs in one or more distributions of the
trigeminal nerve, with no radiation beyond the trigeminal
distribution
- Pain has at least 3 of the following:
• Reoccurring in paroxysmal (sudden and frequent) attacks from a fraction
of a second to 2 minutes
• Severe intensity
• Electric shock like, shooting, stabbing or knife-like
• Precipitated by innocuous (non-harmful) stimuli by the affected side of
the face e.g. washing or shaving area
449
what are the investigations for trigeminal neuralgia?
- In order to diagnose needs to be at least 3 attacks with unilateral facial pain
- Clinical diagnosis based on criteria above and based on history
- MRI to exclude secondary causes or other pathologies
- Not attributed to another disorder
450
what are brainstem lesions caused by?
- Tumour
- MS
- Trauma
- Aneurysm
- Vertebral artery dissection resulting in infarction
- Infection - cerebellar abscess from ear
451
what are the signs of a CN3 palsy?
- Ptosis - dropping eyelids
- Fixed dilated pupil - loss of PARASYMPATHETIC outflow from EDINGER
WESTPHAL NUCLEUS which supply pupillary sphincter and ciliary bodies -
lens accommodation
- Eye down and out
452
what are the causes of CN3 palsy?
* Raised ICP
* Diabetes
* Hypertension
* Giant cell arteritis
453
what are the signs of a CN4 palsy?
Innervate superior oblique muscle and results in a head tilt to correct the
extortion that results in diplopia on looking down e.g. walking downstairs
454
what are the causes of a CN4 palsy?
Trauma to the orbit - rare
455
what are the signs of a CN6 palsy?
Innervate the lateral rectus muscle thus eyes will be adducted
456
what are the causes of CN6 palsy?
* MS
* Wernicke’s encephalopathy
* Pontine stroke - presents with fixed small pupils +/- quadriparesis
457
what are the signs of CN3,4,6 palsy?
- Non-functioning eye
458
what are the causes of CN3,4,6 palsy?
* Storke
* Tumours
* Wernicke’s encephalopathy
459
what are the signs of CN5 palsy?
- Jaw deviates to side of lesion
| - Loss of corneal reflex
460
what are the causes of CN5 palsy?
trigeminal neuralgia (pain but no sensory loss),
herpes zoster,
nasopharyngeal cancer
461
what are the signs of CN7 palsy?
Facial droop and weakness
462
what are the causes of CN7 palsy?
• Bells palsy is the most common lesion of the facial nerve - will see
dribbling out the side of mouth
• Fractures of the petrous bones
• Middle ear infections
• Inflammation of the parotid gland - which facial nerve passes through
463
what are the signs of CN8 palsy?
- Hearing impairment
| - Vertigo and lack of balance
464
what are the causes of CN8 palsy?
• The vestibulocochlear nerve runs very close to the bone
• Is also very affected by surrounding tumours - if a tumour arises in the
internal acoustic meatus then this will press on the vestibulocochlear
& facial nerve
• Skull fracture
• Toxic drug effects
• Ear infections
465
what are the signs of CN9,10 palsy?
- Gag reflex issues
- Swallowing issues
- Vocal issues
466
what are the causes of CN9,10 palsy?
jugular foramen lesion
467
which conditions are associated with berry aneurysms?
- Polycystic Kidney Disease
- Coarctation of aorta
- Ehlers-Danlos syndrome & Marfan syndrome
468
give an example of an SSRI
citalopram
fluoxetine
sertraline
469
what conditions do SSRIs treat?
- first line for moderate to severe depression
- mild depression if other treatments have failed
- panic disorder
- OCD
470
what is the mechanism of action for SSRIs?
SSRIs preferentially inhibit neuronal reuptake of serotonin from the synaptic cleft -> increases availability for neurotransmission
471
what are the side effects of SSRIs?
- GI disturbance
- appetite and weight disturbance
- hypersensitivity reactions
- hyponatraemia
- suicidal thoughts
- seizures
- prolonged QT interval
472
what are the contraindications of SSRIs?
- contraindicated with other monamine oxidase inhibitors -> may cause serotonin syndrome
- other drugs that cause prolonged QT interval
- increase bleeding when used with anticoagulants
473
give an example of a tricyclic antidepressant
amitriptyline
474
what are the indications for using tricyclic antidepressants?
As a second line treatment for moderate to severe depression where SSRIs
are ineffective
475
what is the mechanism of action for tricyclic antidepressants?
- inhibits neuronal uptake of serotonin and noradrenaline from the synaptic cleft -> increase availability for neurotransmission
476
why do tricyclic antidepressants have extensive side effects?
- they block a wide range of receptors
477
what are the side effects of tricyclic antidepressants?
- dry mouth
- constipation
- urinary retention
- blurred vision
- sedation
- hypotension
- arrhythmias
- QT and QRS prolongation
- hallucinations
- sexual dysfunction
478
when are tricyclic antidepressants contraindicated?
- with other monoamine oxidase inhibitors
479
give an example of a benzodiazepine
diazepam
| lorazepam
480
what are the indications for using a benzodiazepine
- First line treatment of seizures and status epilepticus
- Management of alcohol withdrawal reactions
- SHORT TERM treatment of severe anxiety or insomnia
481
what is the mechanism of action for benzodiazepines?
- Benzodiazepines target the GABA-a receptor, which is a chloride channel that opens in response to binding by GABA (the main INHIBITORY NEUROTRANSMITTER)
- opening the channel allows chloride to enter making the cell more resistant to depolarisation
- They facilitate the enhanced binding of GABA to GABA-a receptors and have a widespread depressant effect on synaptic transmission
482
what are the side effects of benzodiazepines?
cause dose dependent drowsiness, sedation and coma
483
when are benzodiazepines contraindicated?
- in elderly
- those with respiratory or hepatic impairment
- neuromuscular disease
- has sedative effects with alcohol, opioids and CYP450 inhibitors
484
what are the side effects of carbamazepine?
- GI disturbance
- dizziness
- ataxia
- hypersensitivity rash
- oedema
- hyponatraemia
485
when is carbamazepine contraindicated?
- prior anti-epileptic hypersensitivity syndrome
| - caution in hepatic, renal and cardiac disease
486
what is the mechanism of action for gabapentin and pregabalin?
it is closely related to GABA
- It binds voltage sensitive Ca2+ channels, where it prevents inflow of Ca2+ and thus inhibits neurotransmitter release
- interfering with synaptic transmission and reducing neuronal excitability
487
what are the side effects of gabapentin and pregabalin?
- drowsiness
- dizziness
- ataxia
488
what are the contraindications of gabapentin and pregabalin?
- renal impairment
| - other sedating drugs
489
what are the side effects of levo-dopa?
```
nausea
drowsiness
confusion
hallucinations
hypertension
```
490
what are the contraindications for levo-dopa?
- take care in elderly
| - caution in CVS disease
491
why is levo-dopa always given alongside a decarboxylase inhibitor (Co-Careldopa)?
- reduce levo-dopa's peripheral conversion before it is able to enter the brain
this reduces nausea and lowers dose required
492
give an example of a dopamine deleting drug
reserpine
493
what are the indications for using a dopamine depleting drug (reserpine)?
- treat dyskinesia in Huntington's
| - can be used as antipsychotic and antihypertensive drug
494
what is the mechanism of action for dopamine depleting drugs (reserpine)?
- irreversibly blocks vescicular monoamine transporter (VMAT)
495
what are the side effects of dopamine depleting drugs (reserpine)?
- nasal congestion
- GI disturbance
- drowsiness/dizziness
- hypotension
- bradycardia
496
what are the contraindications for dopamine depleting drugs?
- asthma
| - CVS disease
497
give an example of MAO inhibitor?
selegiline
| rasagiline
498
what are the contraindications of MAO inhibitors?
- aged cheese and alcohol -> can cause hypertensive crisis
| - antidepressants and adrenaline
499
give an example of ACh inhibitor
rivastigmine
| donepezil
500
what are the indications for ACh inhibitors?
- alzheimers
- Lewy body dementia
- parkinsons
- myasthenia gravis
501
what is the mechanism of action for ACh inhibitors
inhibits ACh breakdown by blocking site of acetylcholinesterase
502
what are the side effects of ACh inhibitors?
- bradycardia
- hypotension
- hypersecretion
- bronchoconstriction
- GI tract hyper motility
- prolonged muscular contraction
503
what are the contraindications of ACh inhibitors?
urinary retention
| CVS disease
504
which nerve root is compressed in sciatica?
S1
505
what are the causes of primary syncope?
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
506
what is bell's palsy?
- acute unilateral facial nerve palsy
507
what is the cause of bell's palsy?
viral infection - reactivation of herpes simplex virus 1 (HSV1)
this leads to swelling of CN VII
508
what is the clinical presentation of Bell's palsy?
- unilateral LMN facial weakness
- altered taste
- post auricular pain - pain behind ears
509
how do you tell the difference between Bell's palsy and a stroke?
- stroke = forehead still innervated - forehead sparing
| - Bell's palsy = both forehead and lower face are affected on one side
510
what are the investigations for Bell's palsy?
- usually a clinical diagnosis
| - can do more investigations to rule out other conditions
511
what is the treatment for Bell's palsy?
- prednisolone
- eye care
- ?antivirals
512
what visual field defect would be caused by an optic nerve lesion?
monocular vision loss
| - loss of vision in one eye
513
what visual field defect would be caused by an optic chiasm lesion?
bitemporal hemianopia
514
what visual field defect would be caused by an optic tract lesion?
- contralateral homonymous hemianopia
515
what visual field defect would be caused by a lesion on one of the optic radiations?
homonymous quadrantanopia
516
where is the primary visual centre located?
calcarine sulcus of occipital lobe
517
what are the 2 components of an intervertebral disc?
- nucleus pulposus
| - annulus fibrosus
518
what are the characteristics of cushing's triad?
- bradycardia
- irregular respirations
- widened pulse pressure
519
what is cushing's reflex?
- nervous system response to increased ICP
- as ICP increases cerebral perfusion pressure (CPP) decreases, resulting in reduced cerebral perfusion
- sympathetic nervous system is activated which increases BP
520
what are the clinical presentation of cushing's reflex?
- cushing's triad - bradycardia, irregular respirations and widened pulse pressure
- hypertension
- headache
- vomiting
- blurred vision
521
what are the investigations for cushing's reflex?
- measure ICP - lumbar puncture or continuous monitoring via catheter in ventricle of brain
- CT/MRI
522
what is the treatment for cushing's reflex?
- mannitol
- duiretics - furosemide
- steroids - methylprednisolone
- sedatives - propofol
- hyperventilation
- elevate head to 30 degrees (reverse trendelenburg position)
- drain CSF
- craniotomy
523
what are the complications of cushing's reflex?
- herniation -> death
| - brain tissue infarction
524
what is the pathophysiology of horner's syndrome?
unilateral damage to the sympathetic chain
525
what are the causes of 1st order horner's syndrome?
stroke, tumours of hypothalamus, spinal cord lesions
526
what are the causes of 2nd order horner's syndrome?
tumours of upper chest cavity, trauma to the neck
527
what are the causes of 3rd order horner's syndrome?
lesions to carotid artery, middle ear infections, injury to base of the skull
528
what are the clinical features of horner's syndrome?
MAPLE
- Miosis
- Anhydrosis
- Ptosis
- Loss of ciliospinal reflex
- Endophthalmos (sunken eyeball)
529
what is the treatment for horner's syndrome?
treat underlying cause
530
what are the investigations for horner's syndrome?
clinical examination
| MRI - detect lesions
531
what is brown-sequard syndrome?
hemisection of the spinal cord
| DCML, corticospinal tract and spinothalamic tract are affected on one side
532
what is the presentation of brown-sequard syndrome?
- DCML = ipsilateral loss of proprioception and vibration sensation
- spinothalamic = contralateral loss of temperature and pain sensation
- corticospinal = ipsilateral spastic paralysis below lesion
533
what are the signs of a vertebrobasilar artery infarction?
balance and co-ordination
534
what are the signs of lateral medullary syndrome in ischaemic stroke?
Sudden vomiting and vertigo
| Ipsilateral Horner’s syndrome = reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia
535
what are the signs of a brainstem infarction?
```
Quadriplegia
Facial paralysis, numbness
Gaze, vision
Coma
Locked in syndrome
Altered consciousness,
Vertigo , vomiting
```
536
what is Todd's palsy?
temporary weakness after a focal seizure in the motor cortex
537
what are the causes of status epilepticus?
- Abruptly stopping anti epileptic treatment
- Alcohol abuse
- Poor compliance to therapy
538
what is the prognosis for huntington's disease?
- poor prognosis
539
what is the most common cause of death for huntington's disease?
Most common cause of death = Pneumonia
Second most common cause = suicide
540
give one differential diagnosis for huntington's disease
Sydenham’s chorea (Rheumatic fever)
541
what are the secondary causes of syncope?
```
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
```
542
what are the clinical features of syncope?
```
Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache
```
543
`what are the investigations for syncope?
Full history and examination
ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome
24 hour ECG if paroxysmal arrhythmias are suspected
Echocardiogram if structural heart disease is suspected
Bloods, including a FBC (anaemia), U&E (arrhythmias and seizures) and blood glucose (diabetes)
544
what is the management for syncope?
avoid triggers in primary syncope.
| management of underlying pathology
Phase 2A revision
flashcards
Decks in class (38)
# Cards
-
PATHOLOGY206
-
IMMUNOLOGY163
-
PHARMACOLOGY172
-
MICROBIOLOGY324
-
ANTIBIOTICS28
-
PUBLIC HEALTH245
-
ENDOCRINE364
-
CARDIO563
-
HAEMATOLOGY251
-
GI270
-
LIVER & FRIENDS306
-
RHEUMATOLOGY338
-
GU292
-
NEURO544
-
RESPIRATORY290
-
Endocrine to work on127
-
cardio to work on244
-
haematology to work on120
-
GI to work on123
-
liver to work on218
-
rheumatology to work on204
-
GU to work on91
-
neuro to work on275
-
respiratory to work on212
-
misc to work on186
-
Endocrine to work on COPY80
-
cardio to work on COPY159
-
haematology to work on COPY62
-
GI to work on COPY119
-
liver to work on COPY137
-
rheumatology to work on COPY133
-
GU to work on COPY92
-
neuro to work on COPY214
-
respiratory to work on COPY166
-
PATHOLOGY COPY79
-
public health COPY135
-
other revision49
-
antibiotic resistance29
