Chronic Neuro Overview Flashcards
(130 cards)
1
Q
What is the definition of a stroke?
How is this different to a TIA?
A
- a sudden onset focal neurological deficit of presumed vascular origin that lasts for > 24 hours
- a TIA is the same thing but lasts for < 24 hours
2
Q
What are the 2 different types of stroke and what causes them?
A
Haemorrhagic:
- caused by vascular rupture, leading to parenchymal / subarachnoid haemorrhage
Ischaemic** (87%)**:
- caused by vascular occlusion or stenosis
3
Q
What are the 2 main causes of ischaemic stroke?
A
-
atherosclerosis and thrombosis
- atherosclerotic plaque narrows blood vessels in the brain
- if plaque ruptures then a thrombus can form
- thrombus completely blocks the artery, reducing blood flow to the brain and causing an area of ischaemia
-
embolism
- a thrombus that has travelled from elsewhere in the body and become lodged in the brain
- usually associated with atrial fibrillation - higher risk of clot formation
4
Q
What causes symptoms to develop in ischaemic stroke?
A
- thrombosis / embolism or stenosis of a blood vessel leads to hypoperfusion of the brain
- the brain becomes deprived of oxygen
- this leads to an ischaemic cascade that results in cell death and symptoms
5
Q
What causes haemorrhagic stroke?
What pathologies can lead to this?
A
- rupture of a blood vessel leads to leakage of blood into the brain
- pathologies that can lead to intracerebral haemorrhage include:
- hypertension
- microaneurysm rupture
- amyloid angiopathy
- arteriovenous malformation
- trauma
- tumours
6
Q
What causes symptoms in haemorrhagic stroke?
A
- rupture of blood vessel leads to leakage of blood into the brain
- the pressure of the blood on the brain causes cell death
- symptoms can occur due to:
- increased intracranial pressure
- reduced cerebral perfusion
- toxic effects of accumulating blood
7
Q
What are the CHA2DS2-VASc score and HAS-BLED scores used for?
A
- CHA2DS2-VASc score is used to assess the risk of stroke in someone with AF
- this is balanced against the HAS-BLED score which is used to assess patient’s risk of bleeding if anticoagulated
- anticoagulation is recommended in a CHADSVasc score of 2 or more
- UNLESS their HAS-BLED score is > 3
8
Q
What are the different categories in the CHA2DS2-VASc score?
A
- C - congestive heart failure (1)
- H - hypertension (1)
- A - age 75 years or older (2)
- D - diabetes mellitus (1)
- S - previous stroke, TIA or TE (2)
- V - vascular disease (1)
- A - age 65 - 74 years (1)
- Sc - sex category - females get 1 point
9
Q
How is HAS-BLED score calculated?
A
- H - hypertension (1)
- A - abnormal renal or liver function (1 point for each)
- S - previous stroke (1)
- B - bleeding (1)
- L - labile INR (1)
- E - elderly (>65 years) (1)
- D - drugs or alcohol (1 point for each)
10
Q
What are the main risk factors for stroke / TIA?
A
- increasing age
- obesity
- hypertension
- diabetes
- smoking
- hypercholesterolaemia
11
Q
In general, what is the presentation of stroke / TIA like?
What is the onset?
A
- sudden onset
- weakness / numbness in the face, arm or leg
- changes in vision
- dizziness and/or loss of coordination / balance
- problems with speech
- specific presentation depends on the area of the brain that is affected
12
Q
What is needed to distinguish an ischaemic stroke from a haemorrhagic stroke?
What are ischaemic and haemorrhagic pointers?
A
- imaging is needed to distinguish between ischaemic and haemorrhagic strokes
Haemorrhagic pointers:
- very severe headache
-
meningism
- triad of headache, neck stiffness and photophobia
- can be caused by inflammation of the meninges OR raised intracranial pressure
Ischaemic pointers:
- AF
- carotid bruit
- ischaemic heart disease
- previous TIA
13
Q
How is the circle of Willis formed?
A
- the brain has a dual circulation
- anterior circulation originates from the carotid arteries
- posterior circulation originates from the vertebral arteries
- where these 2 circulations meet each other, the circle of Willis is formed
14
Q
Which parts of the brain are supplied by the anterior cerebral artery?
A
- this arises from the internal carotid arteries
- they supply the medial aspect of the frontal** and **parietal lobes
15
Q
Which parts of the brain are supplied by the middle cerebral artery?
A
- these arise from the internal carotid arteries
- they supply the lateral hemispheres (temporal + parietal lobes) and subcortical structures
16
Q
What parts of the brain are supplied by the posterior cerebral artery?
A
- these arise from the vertebral arteries
- they supply the occipital lobe and the inferomedial portion of the temporal lobe
17
Q
What is the main difference in symptoms between an anterior cerebral artery (ACA) stroke and middle cerebral artery (MCA) stroke and why?
A
- in both there is contralateral hemiparesis
ACA stroke:
- the legs are affected more than the arms
- ACA supplies the more medial part of the hemispheres
- in the primary motor cortex, the leg is represented more medially
MCA stroke:
- the arms are affected more than the legs
- MCA supplies the more lateral parts of the hemispheres
- in the primary motor cortex, the upper limbs are represented more laterally
18
Q
What are the typical symptoms associated with anterior cerebral artery (ACA) stroke?
A
- contralateral hemiparesis with lower limb affected more than upper limb
- behavioural changes
19
Q
What are the possible symptoms that may occur in a middle cerebral artery (MCA) stroke?
A
- contralateral hemiparesis - upper limb / face affected more than lower limb
- contralateral hemisensory loss
- apraxia
- aphasia
- quadrantopias
- not all of these symptoms will be present - it depends on which areas of the temporal / parietal lobes are affected
20
Q
Why can contralateral hemisensory loss occur in MCA stroke?
A
- the somatosensory cortex is within the parietal lobe and this can be affected
- this is the part of the brain that receives and processes sensory information for the whole body
21
Q
What is meant by apraxia?
Why might this occur in MCA stroke?
A
- apraxia is a problem with the motor planning to perform skilled tasks / movements when asked
- the person understands what is being asked but is unable to carry out the movement
- the parietal lobe is involved in bringing together and combining information needed to perform skilled actions
22
Q
What are the 2 different types of aphasia that can result from MCA stroke?
Which area of the brain must be damaged to produce this result?
A
Receptive aphasia:
- this results from damage to Wernicke’s area in the left temporal lobe
- Wernicke’s area is responsible for speech comprehension
Expressive aphasia:
- this results from damage to Broca’s area in the left frontal lobe
- Broca’s area is responsible for speech production
23
Q
Why can quadrantopias result from MCA stroke?
A
- this occurs due to damage to the optic radiations
- optic radiations carry information from the lateral geniculate nucleus to the primary visual cortex in 2 loops
Meyer’s Loop:
- this is the inferior optic radiation that passes through the temporal lobe
- if cut this causes superior quadrantopia
Baum’s Loop:
- this is the superior optic radiation that passes through the parietal lobe
- if cut this causes inferior quadrantopia
24
Q
What are the typical symptoms associated with posterior cerebral artery (PCA) stroke?
A
-
homonymous contralateral hemianopia
- usually there is macular sparring
-
visual agnosia
- this in an impairment in recognition of visually presented objects due to damage to the visual association cortex (occipital lobe)
25
26
Why does PCA stroke cause homonymous contralateral hemianopia with macular sparring?
* damage to the visual cortex often leads to **macular sparring**
* **macular representation**, which is found at the **posterior pole** of the occipital lobe, is **_disproportionately large_**
* there is also **_dual blood supply_** to the posterior occipital pole through **PCA and MCA**
* dual blood supply and large macular representation means that the **_centre of the visual field is usually spared_** in occipital lobe lesions
27
Why can a posterior circulation stroke affecting the brainstem be so dangerous?
What are the symptoms?
* a brainstem stroke can be **life-threatening** as the brainstem is responsible for **_vital functions_**
* **__**e.g. breathing and heart rate
* symptoms include **_reduced consciousness_** and **_CN pathology_**
* all of the cranial nerve nuclei are present within the brainstem
28
In general what is the role of the cerebellum?
What type of symptoms will be present in a posterior circulation stroke affecting the cerebellum?
* a lesion in one cerebellar hemisphere will cause **motor deficits** on the **_ipsilateral side_ of the body**
* in general, a lesion in the cerebellar hemisphere results in a **_deterioration of coordinated movements_** or a **decomposition of movement**
* the cerebellar hemispheres influence the **_planning and control_ of _precise movements_ of the extremities** and in the **_timing_** of these movements
29
What mnemonic can be used to remember the symptoms of cerebellar damage?
**_DANISH_**
* **D - dysdiadochokinesia**
* the inability to perform rapid, alternating movements
* **A - ataxia**
* ****this refers to problems with gait and posture
* **N - nystagmus**
* **I - intention tremor**
* **S - slurred, staccato speech**
* **H - hypotonia**
* cerebellar lesions produce signs on the **_IPSILATERAL side_***
30
According to the Oxford Classification of strokes, how is a total anterior circulation stroke (TACS) diagnosed?
All 3 of:
* **homonymous hemianopia**
* ****the person sees only one side of their vision (right or left)
* **higher cortical dysfunction**
* ****this includes aphasia, apraxia, agnosia, etc.
* **contralateral sensory or motor deficit**
must be present
31
According to Oxford Classification of strokes, how is a posterior circulation stroke (PCS) diagnosed?
* PCS involves damage to the **_posterior cerebral artery_** or damage in the **_vertebral-basilar circulation_** (affecting **brainstem / cerebellum**)
Need to have any 1 of:
* **isolated homonymous hemianopia**
* **brainstem signs**
* **cerebellar ataxia**
32
According to the Oxford Classification of strokes, how is a partial anterior circulation stroke diagnosed?
Need to have any **_2_** of:
* **higher cortical dysfunction**
* **homonymous hemianopia**
* **contralateral motor or sensory deficit**
33
What is meant by a lacunar stroke (LACS)?
How is this diagnosed according to the Oxford Classification of strokes?
* lacunar infarcts affect small vessels around the basal ganglia, internal capsule, thalamus & pons
* they result from occlusion of a single small perforating artery
Need to have any of:
* pure motor deficit
* pure sensory deficit
* sensorimotor deficit
34
How long does a TIA typically last for?
What symptom do patients often describe?
* typically lasts for **_10 - 15 minutes_** but can last **up to 24 hours**
* TIA may have resolved before you get to examine the patient
* patients describe **_amaurosis fugax_** as ***"like a curtain descending"***
* global events like dizziness and syncope are not typical
35
Why does amaurosis fugax occur in TIA?
* it occurs due to occlusion of the **_retinal artery_**
* this is a branch of the ophthalmic artery, which is a branch of the ICA
* patients describe a **_unilateral progressive vision loss_** as like "a curtain descending"
36
How can the investigations of stroke be divided?
What is the initial approach when stroke is suspected?
***_Hyperacute setting:_***
* stroke is a medical emergency so follow an **ABC approach**
* treatment should NOT be delayed by investigations
***_Subsequent investigations & management:_***
* to reduce risk factors and prevent further strokes
37
What is the first investigation that should be performed in suspected stroke?
Why is this performed and what time limit should it be performed within?
* after initial life support management of airway, breathing and circulation, the next goal is to obtain a brain image
* a **_non-contrast CT head_** is performed to **_rule out a brain haemorrhage_**
* a normal CT scan does NOT rule out ischaemic stroke
* this is **URGENT** and should be performed within **_1 hour_**
38
Whilst non-contrast CT head is being arranged, what blood tests should be performed and why?
What other investigations might be performed at this stage?
* **serum glucose**
* to exclude hypoglycaemia as a cause for focal neurological signs
* **FBC**
* exclude anaemia or thrombocytopenia prior to possible initiation of thrombolytics / anticoagulants
* **U & Es**
* exclude electrolyte disturbances as a cause of focal neurological signs
* look at urea and creatinine to exclude renal failure
* **prothrombin time**
* **cardiac enzymes**
* stroke can be associated with concomitant MI
* vital signs and **ECG** should be performed to **exclude cardiac arrhythmia or ischaemia**
* these are commonly seen in ischaemic stroke
39
Why is it important to perform a non-contrast CT head immediately if stroke is suspected even though ischaemia is not always visible?
* the purpose of the CT head is to **_rule out haemorrhage_** before treating ischaemic stroke
* ischaemic stroke can take **up to 24 hours** to appear on CT so may not always be visible
* treatments used for ischaemic stroke include anticoagulants or thrombolytics, which would make a **haemorrhage worse**
40
Once haemorrhage is excluded, what is the next stage in hyperacute management of ischaemic stroke?
* if it has been **_\< 4.5 hours_ since symptom onset** then **_IV alteplase_** is given
then given **300mg oral aspirin**
* if it has been **_\> 4.5 hours_ since symptom** onset then **_300mg oral aspirin_** is given
* this is also the treatment if thrombolysis is contraindicated
41
What is alteplase?
How does it work to treat ischaemic stroke?
Why can it not be given if \> 4.5 hours have passed since symptom onset?
* it is a **recombinant tissue plasminogen activator (r-tPA)**
* it promotes **_thrombolysis_**, thereby **_re-canalisation_** and **_reperfusion_** to the brain
* after 4.5 hours there is no clear evidence that thrombolysis is effective, whilst there is an **increased risk of intracranial bleeding**
42
When should aspirin be given to ischaemic stroke patients?
* it should be given to **_ALL_** ischaemic stroke patients
* this includes those who have received r-tPA and those who have not
* if r-tPA has been administered, aspirin should **not be started for 24 hours**
* and then only after a CT head has shown no signs of intracranial haemorrhage
43
What are the contraindications for thrombolysis in ischaemic stroke?
* \> 4.5 hours since onset of symptoms
* CT reveals acute trauma or haemorrhage
* symptoms suggestive of subarachnoid haemorrhage
* high INR, APPT or PT
44
Following a stroke, what further management is performed within the stroke unit?
* swallowing assessment
* VTE prophylaxis
* GCS monitoring
* early mobilisation and rehabilitation
45
What other investigations might be considered once a stroke patient has been treated acutely and stabilised?
* **_CT angiogram_**
* should be perfomed in all patients with acute ischaemic stroke and **suspicion of large vessel occlusion** as these would be candidates for **endovascular thrombectomy**
* **MRI / MRA**
* **_carotid doppler_**
* this is used to look for **carotid artery stenosis**
* if **\> 70% occlusion** then **carotid endarterectomy** is recommended
46
What is involved in the secondary prevention of stroke in AF patients and non-AF patients?
* AF patients treated with **_warfarin prophylaxis_**
* non-AF patients **continue aspirin for 2 weeks** then switch to lifelong **_clopidogrel_**
* ***haemorrhagic*** stroke patients need **control of BP** and a **review of anticoagulation medication**
47
Who might benefit from a carotid endarterectomy?
* if \> 70% occlusion is seen on carotid doppler
* if 50-69% occlusion is seen but the patient is symptomatic
48
What is involved in the acute management of haemorrhagic stroke?
* if haemorrhage is seen on initial non-contrast CT head, this is sent for **neurosurgical evaluation**
* most patients are **admitted to ICU** due to frequent need for **tracheal intubation**, invasive **monitoring of BP** or **intracranial pressure**
* anticoagulants / antithrombotics can make bleeding worse so should be discontinued / reversed
49
What are the possible complications of stroke / TIA?
* **aspiration pneumonia**
* **cerebral oedema** and raised ICP
* this is seen in patients with large infarctions affecting the cerebellum or MCA
* **seizures**
* **depression**
* **immobility**
* **DVT**
* **death**
50
What score is used to assess the risk of stroke following a TIA?
**_ABCD2 score_**
* **A - age**
* **B - blood pressure**
* **C - clinical presentation**
* **D - duration of symptoms**
* **D - diabetes mellitus**
* score of 4 or more needs referring to stroke specialist
* score of 6 or more has an 80% chance of stroke within the next 2 days
51
How can the causes of collapse be divided into 2 categories?
***_Syncopal - LOC due to hypoperfusion of the brain:_***
* reflex
* cardiac
* cerebrovascular
* orthostatic
***_Non-syncopal:_***
* epileptic seizures
* non-epileptic seizures
* other
* drugs, alcohol, hypoglycaemia
52
When taking a collapse history, what is it important to ask?
* need to ask about what happened **before, during and after** the collapse
53
What is meant by vasovagal syncope (reflex syncope)?
Why does someone collapse?
* occurs due to **_reflex bradycardia_ +/- peripheral vasodilation**
* it is provoked by **emotion, pain** or **standing too long**
* often in response to a stimulus e.g. seeing a needle
* cannot occur when lying down
54
What would you expect to see before, during and after collapse in vasovagal syncope?
***_Before:_***
* a clear **precipitating factor**
* **pre-syncopal symptoms** including nausea, pallor, sweating and narrowing of the visual field
***_During:_***
* onset is over **seconds** (not instantaneous)
* there may be **brief twitching** of the limbs
* this is clonic jerking due to cerebral hypoperfusion
* **urinary incontinence**
* this is uncommon
***_After:_***
* very **quick recovery** on sitting
* unconsciousness typically lasts for 2 mins
55
What are typical causes of cardiac syncope?
* arrhythmias
* Strokes-Adam attack
* outlet obstruction (AS, HOCM)
* massive PE
56
What features would you look for before, during and after syncope if the cause was arrhythmia?
***_Before:_***
* chest pain and palpitations
***_During:_***
* LOC occurs within seconds
***_After:_***
* rapid spontaneous recovery
57
What is meant by orthostatic syncope?
What are typical causes of this?
* this refers to **_collapse on standing up_**
* **dehydration**
* **drugs** - including antihypertensives
* ANS instability and baroreceptor dysfunction
58
What might occur before, during and after an epileptic seizure?
***_Before:_***
* may have **aura** or there may be **no warning**
***_During:_***
* lasts for **\< 3 minutes**
* twitching
* incontinence
* **_tongue biting_** - this is pathognomonic of epilepsy
***_After:_***
* **slow recovery** with confusion
59
What is an important risk factor to pick up in the history for non-epileptic seizures?
* background history of depression
60
What are some causes of cerebrovascular syncope?
* vertebrobasilar insufficiency
* aortic dissection
* subclavian steal
61
What is the definition of epilepsy?
How is this different to a seizure?
* ***epilepsy*** is a **recurrent** tendency to have **_unprovoked seizures_**
* a ***seizure*** is an **_abnormal paroxysmal discharge_** of **cerebral neurones**
* ***convulsions*** are the **_motor signs_** of electrical discharges
* a seizure is a single event and epilepsy is the disease involving recurrent unprovoked seizures*
62
What is the difference between primary epileptic syndrome and secondary seizures?
* if someone has a seizure, this does NOT mean they have epilepsy
* in ***primary epileptic syndrome*** the cause is **idiopathic** and seizures are **_UNPROVOKED_**
* a seizure that has an **_identifiable cause_** is a ***secondary seizure***:
* tumours
* infection
* inflammation
* trauma
63
In a normal brain, what chemicals are involved in neuronal excitation and inhibition?
How is this altered in epilepsy?
* **_glutamate_** and **_aspartate_** are ***excitatory***
* **_GABA_** is ***inhibitory***
* in a normal brain there is a **balance** between mechanisms that excite the neurones and mechanisms that inhibit the neurones
* this **balance is lost** in epilepsy and there is **_excessive excitation_** of neurones, which leads to **_seizures_**
64
When taking a collapse history, what is the most important thing to ask first?
* when taking a collapse history, first need to establish whether there was a **witness**
65
What are the possible triggers for an epileptic seizure?
anything that alters cerebral excitability
* alcohol
* stress
* flickering lights
* lack of sleep
**_there may be no trigger_**
66
What is might a patient describe happening before their seizure in epilepsy?
**_AURA_**
* this may be described as:
* strange feeling in the gut
* deja vu
* strange smells
* flashing lights
* an aura is part of the seizure itself and can last up to a **few minutes**
* not everyone with epilepsy will experience an aura before a seizure
67
What is the difference between an aura and a prodrome?
What does it suggest if an aura is present?
* an aura is **_part of the seizure itself_** and can last up to a **_few minutes_**
* a prodrome is much rarer
* a prodrome precedes the seizure, but is **_not part of the seizure_**
* a prodrome lasts for a **_few hours_** and manifests as a change in the patient's experience or mood
* if present, an aura suggests that the epilepsy is **focal**
68
What are the typical associated features that occur during an epileptic seizure?
How long does it last for?
* usually an epileptic seizure lasts for **_\< 3 minutes_**
* **incontinence**
* **_tongue biting_**
* **jerking movements**
69
What are the typical features that are present after an epileptic seizure?
* **_slow recovery_**
* post-ictal **myalgia**
* post-ictal **confusion**
* post-ictal **headache**
* there may be **Todd's paresis**
* (post-ictal = the period after an epileptic seizure)*
70
What is meant by Todd's paresis?
How long does it take for symptoms to resolve usually?
* a syndrome associated with **_weakness or paralysis_** of **part or all of the body** **_after a focal-onset seizure_**
* it most commonly affects **one limb** or **one half** of the body
* the post-ictal syndrome can last anywhere from **_minutes to days_**
* complete resolution of symptoms is usually seen within 15 hours
71
What are the 2 different types of seizures?
***_Focal seizure:_***
* this starts from **_one specific part of the brain_** and affects one hemisphere
* sometimes focal seizures can progress and become generalised
* these are focal seizures with secondary generalisation
***_Generalised seizure:_***
* this starts in **_both hemispheres_** at the same time
72
What is meant by a tonic-clonic seizure?
How commonly do these occur in epilepsy?
***_Tonic phase:_***
* the muscles become **stiff**
* there is **straightening** of the body and limbs
***_Clonic phase:_***
* there is **quick and rhythmic jerking** of the body, limbs and head
* tonic-clonic seizures are one of the most common types of seizures in epilepsy*
* there is **first a tonic phase** and **then a clonic phase***
73
What is meant by an absence seizure (petit mal)?
Who tends to get these?
* there is **_sudden and brief cessation**_ in activity with _**rapid return to normality_**
* typically involves **brief staring episodes** with behavioural arrest lasting **_5-10 seconds_**
* there is LOC but **posture is maintained**
* typically affects **children**
74
75
What is meant by a myoclonic seizure?
Who tends to get these?
* there are **_repetitive myoclonic jerks_**
* these are **_sudden, short-lasting jerks_** that can affect a muscle or group of muscles
* they are usually **too short to affect consciousness**
* these are most common in **puberty**
76
What is meant by an atonic seizure?
Who tends to get these?
* also known as a **"drop seizure"**
* there is **_partial or complete loss of muscle tone_**
* usually lasts for **\< 15 seconds**
* loss of muscle control, head may drop and patient slumps or falls forward
* most commonly seen in **children**
77
What symptoms would be expected in frontal lobe epilepsy (focal seizure)?
* **_motor_** symptoms
* **Jacksonian march**
* this is a muscular spasm that spreads from the distal part of a limb to a larger area of the body
* **Todd's palsy**
* this is post-ictal flaccid weakness
* **disinhibition** (involuntary actions)
* *the frontal lobe is involved in controlling **voluntary movement, expressive language** and **higher executive functions***
* *e.g. cognititve skills including emotional expression, memory, problem solving, judgement and sexual behaviours*
78
What symptoms would you expect to see in parietal lobe epilepsy (focal seizure)?
* **_sensory disturbances_**
* including pain, tingling, numbness
* *the parietal lobe receives and processes sensory input, such as touch, pressure, temperature & pain*
* *it is also involved in the perception of body awareness (proprioception)*
79
What symptoms would you expect to see in occipital lobe epilepsy (focal seizure)?
* **_visual phenomena_**
* e.g. spots, lines, flashes
* *the occipital lobe is the visual processing area of the brain*
* *it is associated with distance / depth perception, colour determination, object / face recognition and memory formation*
80
What symptoms would you expect to see in temporal lobe epilepsy (focal seizure)?
* **aura**
* **automatisms**
* e.g. lip smacking, playing with fingers
* **hallucinations**
* *the temporal lobe is involved in processing auditory information and encoding memory*
81
How is epilepsy diagnosed?
What investigations may be performed?
* it is a clinical diagnosis
there must be **2 or more** **_UNPROVOKED seizures_** occurring **\> 24 hours apart**
* other investigations that may be performed include:
* EEG
* bloods
* brain imaging (CT / MRI)
82
Why might an EEG be used to aid diagnosis of epilepsy?
this can be used to determine whether the seizure was **focal or generalised**
* a seizure manifests as a spike
* in a focal seizure there will be spikes only in one part of the brain
* in a generalised seizure, there are spikes everywhere
83
Why are bloods and brain imaging performed when diagnosing epilepsy?
these are performed to **_rule out secondary causes_** of a seizure
***_Bloods:_***
* **blood glucose** - hypoglycaemia can cause seizures
* **FBC** - to evaluate whether there is an infection
* **electrolytes** - disturbances can provoke seizures
* **serum prolactin** - can be transiently elevated following seizures
***_Brain imaging:_***
* to identify potential **structural lesions** which could have precipitated the seizure
84
Why do you want to try and use monotherapy to manage epilepsy?
* the side effects associated with epilepsy medications are very significant
* using only one drug limits the risk of side effects
85
What medications are given to treat focal and generalised seizures?
Which medication is preferred in pregnancy?
***_Focal seizures:_***
* carbmazepine
* lamotrigine
***_Generalised seizures:_***
* sodium valproate
* carbmazepine
***_Pregnancy:_***
* some anti-epileptics are teratogenic
* **_sodium valproate MUST be AVOIDED_**
* **lamotrigine** is preferred
86
What are the side effects associated with anti-epileptics?
* **psychiatric side effects** - e.g. depression
* **weight gain**
* ***lamotrigine*** is associated with ***_Stevens-Johnson syndrome (SJS)_***
* this involves flu-like symptoms that turns to a painful rash that spreads and blisters
* ***carbmazepine*** is associated with ***_neutropenia_*** and ***_osteoporosis_***
87
What is meant by status epilepticus?
What tends to trigger this?
* seizure lasting for **_\> 5 minutes_** or repeated seizures **without recovery or regain of consciousness** in between
***_Triggers:_***
* non-adherence to medication
* alcohol abuse
* OD & toxicity
88
What is involved in the management of status epilepticus?
rapid treatment is required to prevent neurological / systemic pathology
* **secure the airway** and give **100% O2**
* obtain **IV access** and **continuous monitoring** of glucose, sats, BP & ECG
* give **_IV lorazepam_**
* if seizure does not terminate **after 10 minutes**, give more **_IV lorazepam_**
* **_IV phenytoin_**
* transfer to ICU
89
If hypoglycaemia is suspected in status epilepticus then what should be given?
* hypoglycaemia can precipitate status epilepticus and is quickly reversible
* give **_50ml of 50% glucose_** if hypoglycaemia is suspected
* ensure to give **_100mg of thiamine_** alongside the glucose as glucose infusion increases risk of **Wernicke's encephalopathy**
90
What are the potential complications from epilepsy?
* SUDEP - sudden death from epilepsy
* behavioural problems
* fractures (from seizures)
* complications from drugs
91
What is meant by Guillain-Barré syndrome?
* acute **autoimmune demyelinating polyneuropathy** affecting the PNS
* it involves an **_autoimmune_** process **_attacking myelin_** in **_peripheral nerves_**
* the immune cells may also attack **Schwann cells**, which produce the myelin sheath
92
What usually precedes someone developing Gullain-Barré syndrome?
* usually someone has an infection before developing GB 2-3 weeks later
* it is thought that the body generates antibodies against the infection, but these then start to attack the Schwann cells
93
What is involved in the initial presentation of Guillain-Barré syndrome?
How does it progress?
* it usually starts with an **_infection_** - URTI or gastroenteritis
* **_2-3 weeks later_** they develop a **peripheral neuropathy** which **progresses acutely**
* ascending paraesthesia and pain
* symmetrical limb weakness
* autonomic symptoms - such as ileus and urinary retention
* it can progress to affect the **respiratory muscles**, leading to **_respiratory paralysis_**
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What infectious agents are associated with Guillain-Barré syndrome?
***_Viral:_***
* cytomegalovirus
* EBV
* hepatitis B / C
* HIV
***_Bacterial:_***
* campylobacter jejuni
* mycoplasma
***_Other risk factors:_***
* cancer (lymphoma)
* immunisation
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How does Guillain-Barré syndrome typically present as symptoms get worse?
* usually starts with the **hands and feet** having a **_tingling sensation_**
* pain and paraesthesia then **ascends up the limbs**
* **_muscle weakness_ on _both sides_ of the body** makes it difficult to walk or climb stairs
* within **_2 weeks_**, the respiratory system could become paralysed
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What are the signs on examination of Guillain-Barré syndrome?
* **hypotonia**
* **flaccid paralysis**
* weakness / paralysis of muscles with reduced tone
* **fasciculations**
* **altered sensations / numbness**
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What is the main investigation performed in Guillain-Barré syndrome?
**_nerve conduction studies_**
* this will show ***_reduced conduction velocity_ in the PNS***
* this involves measuring the speed of conduction in peripheral nerves, which is reduced in GB due to demyelination
* this is usually sufficient for diagnosis
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What might lumbar puncture and CSF analysis show in Guillain-Barré?
What is ruled out from this investigation?
**_albuminocytological dissociation_**
* there is **_raised protein_** in the CSF but **_normal cell count & glucose_**
* this is a hallmark of demyelinating polyneuropathies
* raised protein shows **CNS inflammation**
* glucose and cell count are normal so this **_rules out CNS infection_**
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What other investigations may be performed in Guillain-Barré syndrome?
***_Bedside spirometry:_***
* should be performed every 6 hours initially to check for **respiratory weakness**
***_Bloods:_***
* anti-ganglioside ABs are present in the Miller-Fischer variant and 25% cases of GB
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What is meant by hydrocephalus?
Who tends to be affected?
* **_excessive accumulation of CSF_** in the **_ventricular system_** of the brain
* this leads to an increase in ICP
* it has a **_bimodal distribution_** as it affects the **young** and the **elderly**
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What are the 2 different categories of causes of hydrocephalus?
***_Non-communicating / obstructive:_***
* this is due to an **_obstruction_ in the flow** of CSF
***_Commmunicating:_***
* the problem is outside of the ventricular system
* there is **_reduced absorption_** of CSF or there is **_increased production_** of CSF
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What are some obstructive hydrocephalus causes?
* stenosis of the cerebral aqueduct or interventricular foramina
* lesions in the 3rd or 4th ventricle
* posterior fossa lesions (tumour / blood) compressing the 4th ventricle
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What are examples of communicating causes of hydrocephalus?
* blockage of venous drainage system, leading to reduced CSF absorption
* tumours
* meningitis (typically TB)
* normal pressure hydrocephalus
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What is meant by normal pressure hydrocephalus?
* idiopathic **_chronic ventricular enlargement_** but without significantly elevated CSF pressure
* there is **excessive production of CSF**, but the **ventricular system also enlarges**
* lumbar puncture shows **_normal CSF pressure_**, but patient will still be **symptomatic**
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What is meant by hydrocephalus ex vacuo?
* there is enlargement of the ventricles but this is **_secondary to brain atrophy_**
* e.g. Alzheimer's dementia
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How can hydrocephalus present acutely and gradually?
***_Acute onset - features of raised ICP:_***
* nausea & vomiting
* headache
* papilloedema
***_Gradual:_***
* cognitive impairment
* unsteady gait
* CN palsies
* this occurs due to increased pressure on the nerves
* double vision
* in babies there is **cranial enlargement** as the fontanelles have not fused yet
* typically presents with **sunset eyes** and skull enlargement
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What investigations are performed in hydrocephalus?
***_CT / MRI head:_***
* this is the first line investigation
* it will show **_ventricular enlargement_** and may show the cause (e.g. tumour)
***_CSF analysis:_***
* may show signs of **infection**
***LP is contraindicated in HIGH ICP***
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What is the difference between spinal cord compression, cauda equina and radiculopathy?
***_Spinal cord compression:_***
* the lesion is within the **spinal cord**
***_Cauda equina:_***
* the lesion is within the **cauda equina**
***_Radiculopathy:_***
* the lesion is within the **nerve root**
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What is the definition of spinal cord compression?
* injury to the spinal cord with **neurological symptoms** depending on the **site** and **extent of injury**
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What tends to cause spinal cord compression in young and elderly people?
* tends to be caused by **_trauma_** in young patients
* tends to be caused by **_chronic conditions_** in the elderly
* ***tumours***
* ***osteoporosis***
* ***corticosteroid treatment***
these often lead to **vertebral compression fractures** due to low energy trauma
* can be caused by **_intervertebral disease_** (disc herniation)
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How does spinal cord compression typically present?
What is the onset like?
* presentation depends on the **level and part of the spinal cord** that is affected
* onset can be **_acute or chronic_** - depending on the cause
* acute - trauma , disc herniation
* chronic - tumours, osteoporosis
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What are the motor symptoms of spinal cord compression?
How do UMN and LMN symptoms present differently and why?
* corticospinal tract is the main motor tract with **UMN starting in the motor cortex** of the brain
* it travels in the spinal cord to **synapse with a LMN within the spinal cord**
* the LMN then innervates the target muscle
***At the site of compression:***
* there is damage to **UMN that has _not yet synapsed_**
* there is damage to **LMNs** that are **_meeting with UMNs_** at the **_specific point_** of compression
* **UMN symptoms** **_BELOW_** the level of the lesion
* **LMN symptoms _AT_** the level of the lesion
* limb weakness (hemiplegia / paraplegia)
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What are the sensory and autonomic symptoms of spinal cord compression?
***_Sensory:_***
* **sensory loss** below a specific level
* this is due to damage of ascending tracts
* **back pain**
***_Autonomic:_***
* constipation
* urinary retention
* erectile dysfunction
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What investigations are performed in spinal cord compression?
***_Radiology:_***
* lateral radiographs of the spine to look for loss of alignment, fractures etc.
* MRI or CT scan
***_Bloods:_***
* FBC
* U&Es
* **calcium**
* immunoglobulin electrophoresis (multiple myeloma)
***_Urine:_***
* look for Bence Jones proteins (multiple myeloma)
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What is meant by cauda equina syndrome?
* **_lumbosacral nerve roots_** that form the **cauda equina** in the spinal canal become **compressed**
* these are the nerve roots that are present after the conus medullaris (end of the spinal cord)
* it presents with **_LMN symptoms_**
* we are now out of the spinal cord, so all the UMNs have synapsed with LMNs
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What commonly causes cauda equina syndrome?
How does it present?
* commonly caused by **_disc compression_** and **_stenosis_** of the spinal canal
* presents with **_LMN symptoms_** and:
* perianal anaesthesia / saddle anaesthesia
* bladder retention
* leg weakness
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What is meant by radiculopathy?
* range of symptoms occurring as a result of the compression of a nerve **_at or near the root_** as it exits the spinal cord
* this can cause pain, numbness, tingling and weakness along the course of that nerve
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What are the potential causes of radiculopathy?
How should it be investigated?
***_Potential causes:_***
* degenerative disc disease
* tumours
* osteoarthritis
* infection
* spondylolisthesis
* forward displacement of a vertebra on the one below, producing pain by compression of nerve roots
***_Investigations:_***
* pain that has **not responded to treatment for 6-8 weeks** should be imaged
* CT / MRI can identify **lumbar disc herniation**
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What is the motor and sensory presentation of radiculopathy like?
***_Motor:_***
* **_LMN symptoms_** for the muscles innervated by this spinal root
***_Sensory:_***
* **_dermatomal pattern_** of pain and numbness
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What is sciatica and how does it present?
* sciatica is a type of **radiculopathy**
* it involves **_lumbosacral nerve root impingement_**
* this results in **pain and tingling** radiating from the **lower back** to the **ipsilateral leg**
* there is **weakness of the calf muscles**
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What is meant by a dissociative seizure and when should it be suspected?
* dissociative seizures represent epileptic seizures but have **no biological correlate**
they should be suspected when:
* **_prolonged duration_**
* history of **abuse, psychological** or **emotional precipitants**
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What are typical UMN signs?
* **hypertonia**
* **hyperreflexia**
* spasticity
* clonus
* positive Babinski sign
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What is meant by spasticity?
* the muscle is **very _tight and stiff_ on passive movement** in a **_velocity dependent_** manner
* the amount of resistance is directly proportional to the speed of passive movement
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What is meant by a positive Babinski sign?
* a blunt object is stroked along the lateral border of the plantar surface of the foot
* a ***normal response*** is **_flexion_ of the big toe** and **_adduction_** of the other toes
* a ***positive Babinski sign*** involves **_extension_ of the big toe** and **_abduction_** of the other toes
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What is meant by clonus?
* a series of contractions which occur when a muscle is suddenly stretched and held in that position
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What are the LMN signs?
* hyporeflexia / areflexia
* hypotonia / atonia
* flaccid muscle weakness or paralysis
* fasciculations
* muscle atrophy
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