Neurology - CBLs/Safe prescribing Flashcards
1
Q
What factors do you need to take into consideration when deciding which anti-epileptic medication is the most appropriate choice?
A
Gender
Age – child bearing
Ethnicity – increased risk of steven johns syndrome in Asian, han Chinese, Japanese and thai origine
Type of seizure
Other medication
Co morbidities
Patient preference
2
Q
What drug treatment options can you use to manage focal temporal lobe epilepsy?
A
According to NICE Guidelines – levetiracetam or lamotrigine should be offered first-line to people with newly diagnosed focal seizures.
If these are unsuitable or not tolerated:
* Oxcarbazepine, sodium valproate and carbamazepine may be used.
3
Q
Management of focal temporal lobe epilepsy
If monotherapy with two of the first-line antiepileptic medications is unsuccessful then…
A
adjunctive treatment may be considered
4
Q
Options for adjunctive treatment include;
A
carbamazepine, clobazam, gabapentin, lamotrigine, levetiracetam, oxcarbazepine, sodium valproate or topiramate.
5
Q
Sodium valproate must not be used in females of childbearing potential. A recent review of antiepileptic drugs in pregnancy by the MHRA advised that ________ and ________ are safer in pregnancy than the other medications reviewed.
A
Sodium valproate must not be used in females of childbearing potential. A recent review of antiepileptic drugs in pregnancy by the MHRA advised that **lamotrigine **and levetiracetam are safer in pregnancy than the other medications reviewed.
6
Q
Which ONE of the following is most likely to interact with the patient’s oral contraceptive to decrease its efficacy
Topiramate
Carbamazepine
Lacosamide
Lamotrigine
Levetiracetam
A
Carbamazepine
7
Q
Focal temporal lobe epilepsy
If a decision was made to start lamotrigine, which ONE of the following is the most important information option that should be provided for the patient?
- DVLA guidelines mean that she is able to drive as soon as she has commenced treatment with lamotrigine
- When she starts treatment she may experience some nausea and diarrhoea
- She should see her GP immediately if she experiences a rash
- Myoclonic seizures may be exacerbated by lamotrigine treatment
- She will need to meet the conditions of the Pregnancy Prevention Programme
A
She should see her GP immediately if she experiences a rash
8
Q
Patients who have had a first unprovoked seizure or single isolated seizure must not drive for __ __________, driving may then be resumed provided the patient has been assessed by a specialist as fit to drive and investigations do not suggest a risk of further seizures
A
Patients who have had a first unprovoked seizure or single isolated seizure must not drive for 6 months, driving may then be resumed provided the patient has been assessed by a specialist as fit to drive and investigations do not suggest a risk of further seizures
9
Q
Can patients with Patients with established epilepsy drive?
A
. Patients with established epilepsy may drive provided they are not a danger to the public and are compliant with treatment and follow up. They must be seizure-free for at least a year and must not have a history of unprovoked seizures. At the point the patient does not meet this criteria so will be unable to drive.
10
Q
What is the skin reaction associated with Lamotrigine
A
Lamotrigine is associated with serious skin reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis. The highest risk is within the first 8 weeks of treatment and is associated with initial doses being higher than recommended and more rapid dose escalation than recommended.
11
Q
Which antiepileptic medications require the patient to be kept on the same brand?
A
12
Q
What is Category 2 and Category 3
A
13
Q
All women and girls on antiepileptic drugs should be offered ____mg of folic acid daily before any possibility of pregnancy. This should be continued until week ____ of pregnancy.
A
All women and girls on antiepileptic drugs should be offered 5mg of folic acid daily before any possibility of pregnancy. This should be continued until week 12 of pregnancy.
14
Q
All pregnant females with epilepsy, whether taking medication or not, should be encouraged to notify the…
A
UK Epilepsy and Pregnancy Register
15
Q
What advice would you give to a patient on anti-epileptics who wanted to breastfeed?
A
Women taking antiepileptic monotherapy should generally be encouraged to breastfeed. If they are on combination therapy or there are risk factors such as premature birth, specialist advice should be sought.
All infants should be monitored for sedation, feeding difficulties, adequate weight gain and developmental milestones.
Primidone, phenobarbital and benzodiazepines are associated with an established risk of drowsiness in breast-fed babies and caution is required
16
Q
Which ONE of the following medications is NOT known to lower the seizure threshold?
A Ciprofloxacin
B Lithium
C Theophylline
D Baclofen
E Gentamicin
A
Gentamicin
17
Q
Status Epliepticus
A decision is made to commence intravenous phenytoin. What dose will you prescribe
A
IV phenytoin loading dose is 20mg/kg followed by maintenance of 100mg every 6-8 hours adjusted according to plasma concentration monitoring. Patient weighs 70kg therefore 70 x 20 = 1400mg
18
Q
How should the intravenous loading dose of phenytoin be administered? How would you advise the nursing staff to prepare the infusion?
A
- Manufacturer advises that each injection or infusion should be preceded and followed by an injection of sodium chloride 0.9% through the same needle or catheter to avoid local venous irritation.
- For IV injection – give into a large vein at a rate not exceeding 50mg/minute (a rate of 25mg/minute may be more appropriate in elderly patients and those with heart disease).
- For intravenous infusion – dilute in 50-100mL sodium chloride 0.9% (final concentration should not exceed 10mg/mL) and give into a large vein through an in-line filter (0.22-0.50 micron) at a rate not exceeding 50mg/minute (again a rate of 25mg/minute may be more appropriate in some patients). Complete administration within 1 hour of preparation.
19
Q
What monitoring is needed whilst intravenous phenytoin is being given?
A
- You need to monitor the patient’s respiratory rate, blood pressure and pulse.
- Phenytoin can cause hypotension and respiratory depression if it is given too quickly.
- You need continuous ECG monitoring o This is because phenytoin can cause arrhythmia. The injection also contains propylene glycol to help improve its solubility and this is potentially cardiotoxic.
- You also need to monitor phenytoin levels. o These should be taken 24 hours after the loading dose o Target is 10-20 mg/L
20
Q
The increased dosage of levodopa can result in a phenomenon known as
A
dopamine dysregulation syndrome,
21
Q
how does dopamine dysregulation syndrome present
A
agitation, aggression, hallucinations, and nausea
22
Q
What are common side effects of levodopa containing medications
A
Postural Hypotension
Nausea and Vomiting
Dyskinesia – abnormal involuntary movements eg twitching, jerking etc
‘on-off’ effect – fluctuations in effectiveness of the medication
Psychosis/hallucinations
Reddish discolouration of urine upon standing
23
Q
When starting a patient on levodopa containing medications – what important safety information must be relayed to the patient/carers?
A
Side Effects: Review common side effects such as nausea, vomiting, dyskinesias, orthostatic hypotension, hallucinations, and mood changes/impluse disorders. Encourage the patient to report any side effects promptly.
24
Q
Which 2 antiemetics would be NOT suitable to treat the PD patient’s nausea? Why?
Metoclopramide
Cyclizine
Domperidone
Ondansetron
Prochlorperazine
A
Metoclopramide
Prochlorperazine
Metoclopramide is a dopamine receptor antagonist and may antagonist the effects of levodopa in the treatment of Parkinson’s disease. It can potentially worsen Parkinson’s symptoms and is generally avoided in patients with Parkinson’s disease.
Domperidone- exception- only works peripherally so it doesn’t cross the BBB
25
How does a patient with adrenal crisis present
The patient's symptoms of fatigue, weakness, nausea, and dizziness, along with the abnormal laboratory findings (elevated potassium and hyponatremia)
26
The immediate management of adrenal crisis would involve:
* Administering Intravenous Hydrocortisone: 100mg stat then 60 mg prednisolne PO
* Correcting Electrolyte Imbalances: Addressing the elevated potassium and hyponatremia through appropriate measures.
* Fluid Resuscitation: If the patient is hypotensive or dehydrated, fluid resuscitation may be necessary.
27
When starting high dose steroids in a patient, what baseline measures should you check?
Calcium vitamin d
Triglycerides
Potassium levels
FRAX score
Vaccination
Chicken pox
Eye Exam
28
3. When starting a patient on steroids, what important counselling points does the patient need to be aware of
Do not stop suddenly
Weight gain is side effect of steroid therapy
Mood changes, anxiety, insomnia, infection gastric upset – side effects
Avoiding infections: as steroids can suppress the immune system. This includes practicing good hand hygiene and avoiding close contact with sick individuals.
Hydration
Medication adherence
Medical alert band
29
What supportive medications would you expect to see prescribed for a patient on long term steroids?
* Calcium and Vitamin D
* Bisphosphonates: pt increase risk of osteoporosis
* PPI – reduce gastric bleeds.
* Antihypertensives – steroids can contribute to blood pressure.
* Psychiatric medication
* PCP prophylaxis – co trimoxzole 960mg 3 times a week
30
5. What advice would you give when starting a bisphosphonate?
* Medication adherence - Typically, these medications are taken orally, usually on an empty stomach, with a full glass of water, and at least 30 minutes before the first food or drink (other than water) of the day.
* Remain Upright After Taking the Medication prevents irration of the oesophagus
* Avoid taking food or beverages for at least 30 minutes after
* Vitamin D and Calcium
* Dental issues: Osteonecrosis of the jaw associated with the drug.
31
Which abx is contraindicated in Myasthenia Gravis
Gentamicin
32
Are you aware of any other medication classes which are to be avoided in patients with MG?
Aminoglycoside Antibiotics:
Fluoroquinolone Antibiotics
Beta-Blockers:
33
What are the likely causes of decline in conscious level after an assault?
- Expanding haematoma, causing brain compression
- Brain swelling
- Seizure
- Scalp laceration causing major haemorrhage and shock
- Possible intoxication
- Not a primary brain injury - too distant from initial injury
34
What does the brain require to maintain consciousness?
* Reticular activating formation within the brainstem, and at least one hemisphere are the minimum two anatomical structures required for the patient to be conscious.
* In health, brain tissue requires glucose and oxygenated blood at a cerebral perfusion pressure (“CPP”) of 50 - 60 mmHg
35
How do you work out CPP
Mean Arterial Pressure (“MAP”) - Intracranial Pressure (“ICP”)
36
How do you calculate MAP
(2x DBP) + SBP / 3
37
What is normal range of MAP
70-100
38
What is normal range of ICP
5-15
39
In what two way can a head injury affect brain function?
Microscopic level
Macroscopic level
40
How could a head injury affect brain function at a microscopic level?
At the microscopic level, the trauma leads to **direct cellular injury** - possibly leading to depolarisation, release of neurotransmitters, or even cell death. The wave of depolarisation spreads and overwhelms normal function and hence consciousness is impaired
41
How could a head injury affect brain function at a macroscopic level?
**Direct Compression to Neurons and Axons:**
* The head injury can cause direct compression to neurons (nerve cells) and axons (nerve fibers).
* Compression can impair the function of these neural structures, affecting the transmission of signals.
**Brain Displacement and Herniation:**
* If the pressure within the skull is very high, the brain can be forced from one anatomical location to another, resulting in herniation.
* Herniation involves marked compression at the site of displacement, causing significant damage.
**Secondary Impaired Blood Supply (Perfusion):**
* Direct compression to the brain tissue or a global increase in intracranial pressure can lead to secondary impaired blood supply, known as perfusion.
* Munro-Kelli mechanism is mentioned, highlighting how cerebrospinal fluid (CSF) and the venous system initially buffer the mass effect. However, when this buffering capacity is exceeded, there is a decompensation.
* Raised intracranial pressure (ICP) resulting from the head injury can lead to reduced blood supply to the brain.
* Reduced blood supply contributes to a decrease in brain function, leading to a reduction in consciousness.
42
What is the most commonly used scale to metric for conscious level? How does it work
Glasgow Coma Scale. Three domains - Eyes, Voice and Movement
43
As part of the examination, you note that the patient now has unequal pupils - the left side is 2 mm reactive and the right side is 7 mm unreactive. What is the cause of this neurological sign?
In this case, the neurological sign is likely to indicate a **herniation syndrome**. Uncal herniation presents with a characteristic ipsilateral pupillary dilation. This is due to direct compression to the 3rd cranial nerve by the herniated temporal lobe. This compression impairs the parasympathetic supply to the eye (as the parasympathetic supply is located the surface of the CNIII and vulnerable to compression) and thence a loss of normal pupillary constriction function. Unopposed sympathetic function leads to a relatively dilated pupil.
44
What is the importance of a unreactive pupil in context of TBI
In a clinical context, a blown pupil is a barometer in to the intracranial pressure and it portends a life threatening deterioration; A herniation syndrome is a neurosurgical emergency.
45
If a patient who comes in with TBI and unreactive pupil, what is the inital management for this patient
The patient should have 1.urgent intubation, 2.osmotherapy (Mannitol or hypertonic saline) and 3.CT scan
46
Surgical intervention for TBI patient
craniotomy and evacuation of the haematoma.
47
What is the relevant anatomy in this case when planning the craniotomy?
The CT appearance is a lens shaped extradural haemorrhage (“EDH”). Normally the dura is tightly attached to the inside of the cranium. Only a high pressure bleed (arterial) has the force to be able to detach the dura from the skull. The bleeding point is at the centre of the haemorrhage and as the haematoma expands it causes further stripping of the dura to give the lens shaped characteristic appearance.
85% of EDHs are from the same artery-** the middle meningeal arter**y. This artery supplies the fragile temporal bone (as little as 2mm thick) and dura. The course of this artery runs in close proximity, often intraosseously, to the pterion and is vulnerable to injury from a skull fracture.
Craniotomy should be centred over the **pterion** to effectively control (ligate) the artery.
Other considerations should be the** location** of the temporal branch of the facial nerve and the superficial temporal artery, both can be avoided by starting the incision close to the tragus. The curved myocutaneous flap is utilised as it is easier to extend than a linear wound and also allows the incision in the hair line for cosmesi
48
What is pterion?
* Pterion is a meeting of cranial
sutures, comprising the frontal,
parietal, sphenoid and temporal
bones.
49
Why is middle meningeal artery vulnerable to fractures?
The middle meningeal artery
has a partially intraossious
course on the inside of the skull
and is vulnerable to fractures
50
What is non epileptic status?
This refers to a prolonged state of continuous or repetitive seizures that is not caused by abnormal electrical activity in the brain. It may be due to various medical or physiological conditions, such as metabolic disorders, drug intoxication, or severe infections. If the patient is being restrained then its non-epileptic. Gaze averision when the eyes move away from where you standing.
51
What is convulsive status epilepticus?
This involves a prolonged state of continuous or repetitive convulsive seizures caused by abnormal electrical activity in the brain. It is a medical emergency and is considered a more severe form of epilepsy
52
How do you distinguish between non-epileptic status and convulsive status epilepticus?
NES - Large amplitude
53
What would PMHx reveal in patients with Non epileptic attacks?
PMHx will often reveal a history of psychological problems in teenage years, including being treated for anxiety and depression, self-harm, including parasuicide, label of emotionally unstable personality disorder and other physical symptoms for which no structural cause has been identified; IBS, fibromyalgia. Patients may fulfil diagnostic criteria for somatic symptom disorder
54
Who gets PNEAD and why?
young woman who have experienced abuse in childhood and who will often subsequently form abusive relationships in adult life. Trauma conditions the brain to dissociate and this is manifest by somatic symptoms.
Trauma early in life conditions the brain to dissociate and this is manifest as somatic symptoms
55
Patients with PNEAD often make compliants about the doctor. What is the role of the neurologist here?
Neurologist therefore has two important roles - firstly, to explain that the symptoms are real but not due to structural disease in the brain (they are not making it up), “the brain is playing tricks on the body” can be a useful phrase, this happens to people at a subconscious level; they are not in control at these times, but, neither are they “mad”;
Secondly, the patient does not have epilepsy and that label, affirmed by taking AEDs, is removed by stopping these drugs. Most patients need to go through a process of investigation (MRI, EEG +/- video monitoring) to confirm the diagnosis although the increasing use of “video clips” on phones does simplify the diagnostic process.
56
Management of PNEAD
Neuropsychologists will explore with the patient whether they can make a connection between remote trauma and current symptoms and then use some form of therapy to help them to cope. Symptoms can get worse before they start to improve, and these patients remain vulnerable to relapse at times of stress. Some patients also need anxiolytic or antidepressant medication.
57
Can non epileptic attacks happen in adults?
Non-epileptic attacks can also occur in older individuals; the key differences are that they occur as commonly in men as in women, and in DS experience, are typically triggered by life-changing physical health problems. These patients often have insight into the origin of the problem and are responsive to psychological interventions.
They are called **Late-onset psychogenic non-epileptic attacks**
58
What is status epileticus
SE is defined as > five minutes of continuing seizure activity or repetitive seizures without regaining consciousness between episodes.
5-minute threshold is a practical clinical guideline, and individual cases may vary. Some guidelines may define status epilepticus with a shorter or longer duration
59
Seizure Initiation: Patho
**Milliseconds:** During a seizure, there are rapid changes in the opening and closing of ion channels, leading to the release of neurotransmitters (NT).
**Early Events (Seconds to Minutes):** Receptor Trafficking: There is a movement of receptors, specifically GABA receptors, into the cell.
**NMDA Receptor Overactivity:** NMDA receptors (a type of glutamate receptor) become overactive. Glutamate is a major excitatory neurotransmitter in the brain.
**Calcium Influx:** Calcium ions enter the neurons. Excessive calcium influx is a key event in excitotoxicity.
**Cascade of Processes: **The excessive calcium triggers a cascade of biochemical processes within the neuron.
**Cell Death Pathways:**
Necrosis: Uncontrolled cell death.
* Apoptosis: Programmed cell death.
* Long-term Structural Damage:
The culmination of these processes can lead to long-term structural damage to the affected neurons
60
What is the management of convulsive status epilepticus?
* Ongoing management
* Bloods
* ECG
* Treat systemic problems; hypoglycaemia, acidosis, infection
* Resume treatment epilepsy
* Identify underlying cause
61
What is refractory status epilectus?
Refractory SE is defined as ongoing seizures despite two I.V treatments, one of which is a benzodiazepine.
: If seizures continue for 30 minutes despite first line (benzodiazepine) and second line (see slide 34) treatment, the patient has refractory status epilepticus and should be managed on ITU
62
63
Initial management of SE
The first specific treatment is 4 mg of I.V Lorazepam
then after 5-10 minutes adminster again if seziures have not stopped
Then use either sodium valporate, keppra or phenytoin
64
What information do you need to find out if patient with SE is known to have seizures?
You will want to know about his usual seizure control, his medication, and, in particular, compliance with AEDs, working out how to access information about his epilepsy also very important.
Examination should focus on whether or not he has a neurological deficit and whether or not there is evidence of intercurrent infection. Investigation should include a blood sample for AED levels. In most instances, a brain scan will not be needed. '
His usual medication should be started as soon as this is known, making sure that a sample for levels has already been taken. SE in a patient with epilepsy due to poor compliance with medication / low AED levels has a good prognosis.
65
What information do you need to find out if patient with SE is not known to have seizures?
While an idiopathic / cryptogenic epilepsy can present with SE, in the absence of a previous history of epilepsy, a serious structural intracranial or systemic encephalopathy is much more likely. Structural causes include: stroke - acute or remote (especially in the elderly), infection (common and rare organisms, think about recent travel), trauma (recent, remote), inflammatory (often autoimmune) and systemic causes include drugs, e.g. cocaine, alcohol including withdrawal, anoxia, hypoglycaemia, severe electrolyte disturbance and there are many rare causes (beyond the scope).
66
What does tetraparesis mean? Is another word you can use interchangably
Tetraparesis means weakness in all four limbs. It is synonymous with quadriparesis (“tetra” and “quadri” are simply derived from Greek and Latin for “4” respectively).
67
What does pelgia mean?
Plegia would be complete paralysis or loss of power, rather than graded weakness but there is no clinical significance to the difference in use of “paresis” and “plegia.”
68
What does polyneuropathy mean?
Certainly! Polyneuropathy is a condition that involves damage or dysfunction of multiple peripheral nerves in the body. Let's break down the term:
**Poly-:** This prefix means "many" or "multiple."
**Neuropathy: **"Neuro" refers to nerves, and "pathy" means disease or abnormal condition.
So, polyneuropathy essentially means a situation where many nerves throughout the body are affected by some form of damage or dysfunction.
69
There are forms of meningeal infection that can mimic forms of polyneuropathy. What are they?
chronic meningitis, from Lyme disease or from viral infections
70
What is the well known trigger for GBS
In addition to the timing of the neurological syndrome being typical, we have corroborating evidence from the previous **campylobacter infection**. This is the most well known trigger for the GBS, through **molecular mimicry and antigen cross reactivity**. Although diarrhoea is the most classical prodromal illness, before GBS, other infective symptoms are often described. In many patients, no prodrome can be identified.
71
What tests were used to confirm the clinical diagnosis of GBS?
This is a clinical diagnosis, but supportive tests are certainly relevant.
The two most relevant tests are NCS / EMG and CSF.
Nerve conduction studies are useful to confirm the diagnosis
72
What would you see in CSF analysis for GBS
In CSF analysis, the key feature would be high protein (albumin) levels with the absence of cells, known as cyto-albuminic dissociation. If cells are present, these could denote a primary infection or a neoplastic problem rather than primary autoimmunity. CSF protein levels become elevated in GBS (though usually only after some days from symptom onset); in practice, this is a useful confirmatory finding.
73
Nerve conduction studies are useful to confirm the diagnosis, and may distinguish between...
peripheral nerve axonal disease and peripheral nerve demyelinating disease.
74
The classical picture in GBS is ____________, leading to the alternative abbreviation AIDP (acute inflammatory demyelinating polyradiculoneuropathy).
The classical picture in GBS is **demyelination**, leading to the alternative abbreviation AIDP (acute inflammatory demyelinating polyradiculoneuropathy).
75
What would you see in nerve conduction studies for GBS
In this case, one would see preserved amplitudes on the NCS but delayed conduction velocity and sometimes conduction block. Slow conduction is of course very easy to map on to our preclinical knowledge of the function of the myelin (which is damaged in GBS), namely to improve the speed of conduction of the neural impulse. Conduction block is rather more difficult to conceptualise but is thought to result from failure of a neural impulse to “jump” from one node of Ranvier to the next. As such, like delayed conduction, conduction block is a pointer towards impaired function of peripheral nerve myelin.
76
What is the five-day course of treatment for GBS
Intravenous immunoglobulin is used to modify the autoimmune response that causes peripheral nerve damage in GBS. Plasma exchange has similar efficacy. Steroid treatment in AIDP has been shown to cause more harm than benefit. However, oral immunomodulatory medications, including steroids (and the so-called steroid-sparing agents) may be used in conditions related to GBS, namely CIDP (chronic inflammatory demyelinating polyneuropathy).
77
What is the first priority in a patient with GBS?
The first priority in GBS is the patient's safety, and the most important function is breathing. Progressive impairment in ventilation, potentially leading to respiratory arrest, is characteristic of GBS. Although not all patients experience the disease in so severe a form, all must be monitored carefully, by measuring FVC (at least in normal times, although the aerosol-generating potential of spirometry is a safety consideration which has been to the fore in 2020).
78
What are some respiratory complications of GBS
Respiration is likely to have been compromised in this case by **hypoventilation**, from dysfunction of the nerves passing to the diaphragm and the accessory muscles of ventilation. The patient might also have **aspiration pneumonia** as a result of neuromuscular impairment of** safe swallowing**. By being immobile, the patient is also at risk of **DVT,** and consequently at risk of pulmonary embolism. Death may occur from any of these complications. Mechanical ventilation, antimicrobial treatment and / or anticoagulation could be life-saving
79
List some of the possible non-respiratory complications in GBS
Risks include** trauma** (e.g. to eyes, teeth / mouth, skin, urthethra). A major risk to skin integrity comes from pressure effects, suboptimal nutrition, and maceration from excretions. **Infection** and **sepsis** are possible, with origin in the respiratory system or from a site of instrumentation. Nutritional impairment could increase the risk of **peptic ulcer**. Mechanical complications might occur in relation to posture, e.g. **shortening of gastrocnemius** tendon (if feet not in dorsiflexion), and in relation to the early recovery (**ulnar palsy** if moving on elbows, falls when he starts to ambulate). Pain and adverse effects of medication for pain are highly relevant, as might be **delirium and depression.**
80
What would be the difference between a patient with classical locked-in syndrome and a patient with a severe GBS?
A patient who has a complete polyneuropathy involving paralysis of all muscles, and failure of autonomic output would be absolutely de-efferented - unable to move at all. By contrast, in locked-in syndrome (from pontine infarction), the patient would retain the ability to undertake vertical eye movement and eyelid opening (as these are functions of the neural outflow of the midbrain (C.N. III and IV) and of the vertical gaze nucleus in the midbrain. By contrast, in locked-in syndrome, functions of the pons (which include horizontal gaze) and cerebral control of functions that localise caudal to the pons, would all be affected.
81
On the Rehabilitation Unit, who will be involved in care of GBS patient?
- Occupational therapists,
- Physiotherapists
- Speech and Language Therapists
- Nurses and health care assistants
- Psychologists
- Rehabilitation doctors
- Vocational rehabilitation specialists
82
56-year-old hypertensive, type II diabetic patient is found slumped at home.
What are the differential diagnoses of the cause this decline?
- Surgical sieve: VITAMIN E
- **Vascular CNS**: haemorrhagic / embolic Peripheral event - AAA rupture, MI
- **Infective / inflammatory:** Sepsis, meningo-encephalitis, COPD
- **Trauma CNS: **Concussion, bleed Fracture NOF / rhabdomyolysis
- **Autoimmune CNS / PNS:** Myasthenia, GBS, Hypothyroidism
- **Metabolic:** Hypogylcaemia, hepato-renal failure, **Iatrogenic:**Antihypertensives, benzodiazepines, βblockers
- **Neoplastic:** CNS tumour - seizure / hydrocephalus
- **Environment:** Carbon monoxide, hypothermia, ETOH, recreational, paracetamol, insulin overdose,
83
What does the brain require to maintain consciousness?
Brain tissue requires glucose and oxygenated blood at a cerebral perfusion pressure (“CPP”) of 50 - 60 mmHg.
- CPP = Mean Arterial Pressure(“MAP”) - IntraCranial Pressure (“ICP”)
- A head injury can cause brain oedema, which increases intracranial pressure (“ICP”)
Reticular activating formation (“RAS”) and at least one hemisphere are the minimum two anatomical structures required for the patient to be conscious.
84
By what mechanism do the ‘VITAMIN E’ pathologies affect consciousness?
Any of the surgical sieve pathologies can affect consciousness by:
1) metabolic effects (hypoxia / hypoglycaemia / metabolite build-up / toxicity) causing cellular dysfunction
2) physiological effects alter perfusion (hypotension / acidosis / bradycardia).
3) direct anatomic disruption of the CNS (RAS or hemispheres) by trauma / stroke / infection.
85
56-year-old hypertensive, type II diabetic patient is found slumped at home.
Describe the management steps.
Management = Assessment, diagnosis and instigating treatment
ABCDE
A: Assessing C-spine (it trauma) and GCS with A is useful as a confused patient talking is demonstrating some airway patency
B: In this case no real respiratory issues - **right apical creps** may indicate possible aspiration ABG. No naso pharangeal tube because they might have a skull fracture
C: Obvious hypertensive emergency / malignant hypertension. Cool / hypoperfused peripheries is a manifestation of increase sympathetic function ( α 1 adrenoceptor mediated vasoconstriction)
D: Left face forehead-sparing weakness - UMN aetiology - with left arm and leg weakness, this looks like a stroke. Ophthalmology suggests chronic uncontrolled hypertension (hard exudates and flame haemorrhages)
E: BM 9, otherwise non-contributory
Problems: Acute CNS event, hypertension, possible aspiration, mild hyperglycaemia.
In this context the stroke is likely to be a intracerebral haemorrhage.
**CT brain** required to confirm diagnosis and **antihypertensive** medications required - **labetolol** infusion in HDU advisable as easy to titrate and control
- want to avoid profound hypotension seen with nitroprusside and GTN.
86
What do you call a BP that is 230/100,
Malignant HTN
87
What do you see in the opthalmascope
Papilodeoma- optic disc should be defineced but it is blurred here.
88
Describe this CT head
- Axial CT of the head which is abnormal
- There is a right sided hyperdensity
- located in the basal ganglia
- This CT has mass effect but no midline shift.
- Calcified Choroid seen in ventricles
89
Conservative management of intracerebral haemorrhage
Rehabilitation as per stroke management – multi-disiplinary approach: psychological support and skin management (nursing), swallow and communication assessment (SLT), cognitive assessments (O.T), mobilising (physiotherapy), nutrition (dietetics).
90
Medical Management of intracerebral haemorrhage
INTERACT-2 trial suggests that blood pressure control (systolic target 150 mmHg) limits haematoma expansion, but doesn’t cause any secondary ischaemic events. Other trial with more aggressive blood pressure reducing regimens have led to secondary hypoperfusion infarcts - this is because the cerebrovascular autoregulation is set to a higher blood pressure requirement in chronic hypertensives. Reversal of warfarin (not antiplatelet therapy) improves survival
91
Surgical Management of intracerebral haemorrhage.
Multiple neurosurgical trials looking at clot removal have failed to show significant neurological improvement (STITCH, MISTIE). The only role for surgery currently is for clot removal if there is mass effect causing a life-threatening herniation syndrome
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56-year-old hypertensive, type II diabetic patient is witnessed to suddenly decline, with severe headache, nausea and intermittent vomiting.
What pathologies present is such a rapid (hyper-acute) manner?
Electrical
Vascular
Aterial Haemorrhafe
Hypoperfusion (shock)
Trauma
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What pathologies present in an acute way (minutes to hours)
History is often over hours for systemic metabolic pathologies (sepsis), over hours to days for meningitis, and days for a cerebral abscess. Venous bleeding (such as in acute subdural haemorrhage) presents over this time scale.
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What pathologies present in a Sub-acute: days to weeks?
Days to weeks tends to be the presentation of tumours, hydrocephalus and chronic subdural collections.
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56-year-old hypertensive, type II diabetic patient is witnessed to suddenly decline, with severe headache, nausea and intermittent vomiting.
What is the next diagnostic step?
The priority is to exclude subarachnoid haemorrhage (“SAH”) as a cause, as SAH is a time-critical pathology that requires specialist management. The way to achieve this is with a **CT brain**, performed within **12 hours **it has > 98% sensitivity.
A “thunderclap” headache (maximal intensity within a second) and no blood seen on the scan would mandate a **lumbar puncture after 12 hours** to allow the haemoaglobin ring to be metabolised to the yellow-coloured bilirubin (xanthachromia). The deliberate delay in lumbar puncture (“LP”) allows the clinician to differentiate between the blood released by subarachnoid haemorrhage from bleeding caused by a traumatic LP.
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What is a spontaneous subarachnoid haemorrhage?
A spontaneous subarachnoid haemorrhage is a bleed into the CSF space surrounding the brain.
80% of spontaneous bleeds arise from an aneurysm (a focal weakness and dilation often called a
saccular aneurysm cf AAA fusiform aneurysm). The aneurysm occurs at sites of turbulent flow, so are most common at junctions ACA-ACOM, ICA-MCA, MCA bifurcation. The diagnosis is made by an angiogram. The other 20% where an angiogram shows no aneurysm (“angio-negative”) are from small venous sources, often these occur around the brainstem and are generically referred to as perimesencephalic bleeds.
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What are the principles of management of a patient with confirmed spontaneous subarachnoid haemorrhage?
1. Identify the presence of an aneurysm and to secure it to prevent it bleeding again. The U.K-run ISAT trial has shown that endovascular **coil embolization** of a simple aneurysm is a safer method than open brain surgery to place a clip across the aneurysm. Coiled aneurysms tend to recur more often than surgical clipped, but have the advantage of lower mortality and morbidity for patients. The coiling technique involves a small incision in the groin to access the femoral artery. Then a catheter is fed up retrograde up the aorta to the cerebral vessels. When the catheter is in place, a small platinum coil is positioned and detached in to the aneurysm sac, where it causes a clot and this blocks off the aneurysm from the “parent” vessel
2. To anticipate and manage the sequelae of having the bleed, including: cardiovascular, endocrinolgical, hydrodynamic and neurological problems. If clinical vasospasm occurs, the clinician can increase the MAP to 90 – 100 mmHg to force blood through the narrowed vessels. Occasionally, angioplasty or intraarterial nimodipine are used to relieve a focal spasm.
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CT shows a left-sided frontal acute subdural collection. There is a mass effect (compression of gyri and loss of CSF from sulci) and the is midline shift (evidenced by the septum pellucidum being shifted to the right).
The blood is “acute” as if is hyperdense - so x-rays have been absorbed by the iron in the haem.
It is located in the subdural space as the shape of the collection is a crescent that follows the contours of the brain - cf an extradural (“EDH”), where it is A lens-shaped collection. Also, the history of minimal trauma and anticoagulation lends itself to a subdural location (EDH is usually a young high velocity injury).
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Tx for frontal acute subdural
Operative (craniotomy) or conservative (Observation of neurology, SLT assessment, reversal of anticoagulation, falls work-up).
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How do you assess if patient is fit for surgery?
1) Patient-related factors
These are the patient’s wishes - may not want surgery and, if capacitous, may not want intervention. If the patient lacks capacity, we treat the patient with “best interests”, involving the family. Other important patient-related factors are the fitness for anaesthesia, co-morbidities and baseline function. Usually, an acute subdural will leave the patient with a deficit in cognition and possible mobility issues. These are important considerations before embarking on surgery - a patient with terminal cancer, advanced dementia or end-stage COPD is likely to have a poor recovery from surgery. A decision to not operate is often more difficult and it requires a skilled dialogue with the referring team and the family.
2) Pathology-related factors
Removal of the haematoma is primarily indicated to reduce the associated increase in ICP that is seen with an expanding mass (see Monro-Kellie in TBI CBL). Importantly, there is likely to be brain damage underlying the clot (contusion) so much of the neurological deficits may not resolve.
A very large haematoma (> 20 mm of midline shift) is likely to indicate a poor prognosis (as sheering stress on the midbrain / diencephalon is severe).
3) Neurological-related factors
* Specifically, presenting neurology - a poor presenting GCS portends to a poor outcome.
* Change in symptoms - a rapid decline usually pushes towards surgical intervention.
* Length of symptoms - longstanding symptoms often point to towards relative stability, so conservative measures may be safer than the intervention
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Q3. The patient remains stable and is treated conservatively. However, three weeks later, the patient presents with a rapid decline, with a GCS 3/15. What are the next steps in terms of management?
Management steps - change in status, so re-assess ABCDE and repeat the CT scan.
GCS 3 means that the patient is likely to have an unsafe airway so needs intubation and ITU as a definitive place of care. A CT is urgent as compression to neurological tissue is a time-critical pathology, especially if there is a prospect to remove said compression
