Neurology Final Flashcards

(61 cards)

1
Q

What are is the mx of brain abscess? [3]

A

surgery
* a craniotomy is performed and the abscess cavity debrided
* the abscess may reform because the head is closed following abscess drainage.

IV antibiotics: IV 3rd-generation
* cephalosporin + metronidazole

intracranial pressure management:
* dexamethasone

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2
Q

Describe how you manage NPH [2+]

A

Shunt Surgery
- Ventriculoperitoneal shunting is the most common surgical intervention, with adjustable valve systems preferred due to their ability to regulate cerebrospinal fluid flow based on individual patient needs.
- First-line treatment in the acute setting is usually insertion of an external ventricular drain
- Regular monitoring post-surgery is important to detect complications such as infection, overdrainage, underdrainage, and mechanical shunt failure.

Non-Surgical Management
* While shunting is the primary treatment modality, non-surgical options may include lifestyle modifications such as avoiding medications that can exacerbate symptoms (e.g., sedatives, anticholinergics).
* Physiotherapy may be beneficial in managing gait disturbances.

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3
Q

What investigations do you conduct for MG [4]

A

Ztf:
.1. Antibody testing:
- AChR antibodies (around 85%)
- MuSK antibodies (less than 10%)
- LRP4 antibodies (less than 5%)

.2. A CT or MRI of the thymus gland is used to look for a thymoma.

.3. Edrophonium test:
- Patients are given intravenous edrophonium chloride
- Normally, cholinesterase enzymes in the neuromuscular junction break down acetylcholine. Edrophonium blocks these enzymes, reducing the breakdown of acetylcholine
- As a result, the level of acetylcholine at the neuromuscular junction rises, temporarily relieving the weakness.
- A positive result suggests a diagnosis of myasthenia gravis.

PM:
Repetitive nerve stimulation (RNS):
- repetitive electrical stimulation of a peripheral nerve while recording the compound muscle action potentials (CMAPs) from a target muscle.
- A decline in the amplitude of CMAPs after repetitive nerve stimulation, known as decrement, supports the diagnosis of MG.

Single-fiber electromyography (SFEMG):
- This is the most sensitive test for MG, which measures the variability in the time it takes for individual muscle fibres to respond to nerve stimulation (jitter) and the failure of some fibres to respond at all (blocking).
- Abnormal jitter and blocking are indicative of impaired neuromuscular transmission in MG.

NB:
- due to the potential side effects and limited specificity, edrophonium test has been largely replaced by more specific and sensitive diagnostic tests.

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4
Q

Describe 4 treatment options for MG [4]

A

Pyridostigmine is a cholinesterase inhibitor that prolongs the action of acetylcholine and improves symptoms. First-line

Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies

Thymectomy can improve symptoms, even in patients without a thymoma

Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail

Intravenous immunoglobulin (IVIg) or plasma exchange may be considered in severe cases or during myasthenic crisis.

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5
Q

How do you investigate for LES? [1]

A

EMG
- incremental response to repetitive electrical stimulation

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6
Q

How do you differentiate LES vs MG? [3]

A

Clinically, LES typically presents with proximal muscle weakness that improves with repeated use (unlike MG where symptoms worsen with use).

Autonomic symptoms such as dry mouth or impotence are common in LES but rare in MG.

Ophthalmoplegia and bulbar symptoms are less common in LES compared to MG.

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6
Q
A
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7
Q

Management of Myasthenic Crisis? [2]

A

In a myasthenic crisis, immediate hospitalisation is required.
Intensive respiratory support may be necessary, including intubation and mechanical ventilation if there is impending respiratory failure.

Rapid short-term symptom control can be achieved by plasma exchange or IVIg.

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8
Q

In MG Resp. crisis - what investigation would you do and how would this inform your mx plan? [2]

A

Assessment: BEDSIDE SPIROMETRY - FVC (not peak flow/FEV1):
- >20ml/kg (1.5-2.0L) – on repeated measures – ABG and Rapid response/anaesthetic review – consideration of HDU/ITU
- >15ml/kg (1L) – urgent Rapid response/anaesthetic review and ITU transfer

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9
Q

With Horners, anhydrosis determines the site of the lesion. The causes can be remembered as the 4 Ss, 4 Ts and 4 Cs.

Describe the causes of these lesions [+]

A

Central lesions (4 Ss):
* S – Stroke
* S – Multiple Sclerosis
* S – Swelling (tumours)
* S – Syringomyelia (cyst in the spinal cord)

Pre-ganglionic lesions (4 Ts):
* T – Tumour (Pancoast’s tumour)
* T – Trauma
* T – Thyroidectomy
* T – Top rib (a cervical rib growing above the first rib above the clavicle)

Post-ganglionic lesion (4 Cs):
* C – Carotid aneurysm
* C – Carotid artery dissection
* C – Cavernous sinus thrombosis
* C – Cluster headache

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10
Q

Describe a key test / feature of early stage frontotemporal dementia? [1]

A

Constructional apraxia i.e. failure to draw interlocking pentagons may be a key feature in the early stages

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11
Q

Describe how epilepsy can be classified based on epilepsy syndromes [4]

A

An epilepsy syndrome is determined by a group of features observed together, such as the type of seizure, age of onset, EEG findings, and often prognosis. E.g:

Childhood Absence Epilepsy (CAE):
- Characterised by typical absence seizures, with onset usually between 4-10 years.

Juvenile Myoclonic Epilepsy (JME):
- Marked by myoclonic jerks, typically shortly after waking.

Dravet Syndrome:
- Severe epilepsy beginning in infancy, initially presenting as prolonged seizures with fever.

Lennox-Gastaut Syndrome:
- Characterised by multiple seizure types, cognitive dysfunction, and a specific EEG pattern.

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12
Q

abscence seizures are associated with which findings on EEG? [1]

A

3hz spikes on EEG

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13
Q

Describe the notable side effects of:
- Sodium Valproate [4]
- Carbamazepine [3]

A

Sodium Valproate:
* Teratogenic, so patients need careful advice about contraception
* Liver damage and hepatitis
* Hair loss
* Tremor

Carbamazepine:
* Agranulocytosis
* Aplastic anaemia
* Induces the P450 system so there are many drug interactions

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14
Q

What are notable side effects of:
- Phenytoin [3]
- Ethosuximide [2]

A

Phenytoin
* Folate and vitamin D deficiency
* Megaloblastic anaemia (folate deficiency)
* Osteomalacia (vitamin D deficiency)

Ethosuximide
* Night terrors
* Rashes

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15
Q

Which of the following can cause secondary angle closure glaucoma

Carbamazepine
Lamotrigine
Levetiracetam
Sodium valproate
Topiramate

A

Which of the following can cause secondary angle closure glaucoma

Carbamazepine
Lamotrigine
Levetiracetam
Sodium valproate
Topiramate

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16
Q

What are treatment options for IESS? [3]

A

Steroids
Vigabatrin
+/- ACTH

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17
Q

Describe what is meant by self-limited epilepsy with centrotemporal spikes (SeLECTS)

Describe the presentation

Describe the EEG

A

Presentation:
- 4-10 years old
- Focal seizures are brief, typically < 2/3 mins, few from sleep, associated with somatosensory symptoms

EEG:
- High amplitude centrotemporal sharp and slow wave complexes

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18
Q

Lecture

What is important to know aboout acute ( < 48 hr metabolic / toxic) ir ( < 7 days stuctural), remote ( > 7days from brain insult) with regards relationship with reoccurence and to epilepsy? [2]

A
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19
Q

Lecture:
- Behavioural changes are common with which drug? [1]

A

Levetiracetam

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20
Q

The patient’s presentation of peripheral neuropathy, lymphadenopathy, and bleeding gums suggests that he has been taking which anti-epileptic? [1]

A

The patient’s presentation of peripheral neuropathy, lymphadenopathy, and bleeding gums suggests that he has been taking phenytoin

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21
Q

It is useful when thinking about the management of epilepsy to consider certain groups of patients.

Which patients are have special considerations and how do you manage these? [3]

A

patients who drive:
- generally patients cannot drive for 6 months following a seizure.
- For patients with established epilepsy they must be fit free for 12 months before being able to drive

patients taking other medications:
- antiepileptics can induce/inhibit the P450 system resulting in varied metabolism of other medications, for example warfarin

women wishing to get pregnant:
- antiepileptics are generally teratogenic, particularly sodium valproate.
- It is important that women take advice from a neurologist prior to becoming pregnant, to ensure they are on the most suitable antiepileptic medication.
- Breastfeeding is generally considered safe for mothers taking antiepileptics with the possible exception of the barbiturates

women taking contraception:
- both the effect of the contraceptive on the effectiveness of the anti-epileptic medication and the effect of the anti-epileptic on the effectiveness of the contraceptive need to be considered

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22
Q

Describe the clinical features of ataxic telangiectasia [4]

A

cerebellar ataxia
telangiectasia (spider angiomas)
IgA deficiency resulting in recurrent chest infections
10% risk of developing malignancy, lymphoma or leukaemia, but also non-lymphoid tumours

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23
Q

Describe the differences betwen Freidrich’s ataxia and ataxic telangiectasia? [+]

A

FA:
- HOCM
- DM
- Onset at 10/15 yrs
- Optic atrophy
- Kyphoscoliosis

AT:
- Telangiectasia
- IgA deficiency –> recurrent chest infections
- Increased risk of leukaemia and lymphoma
- Onset at 1-5

NB: both autosomal recessive; cerebellar ataxia and onset in childhood

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24
What are the two most common presenting features of Friredrich's ataxia? [2] Describe the neurological [4] and other [3] features of Friedrich's ataxia
The typical age of onset is **10-15 years old**. **Gait** **ataxia** and **kyphoscoliosis** are the most common presenting features. **Neurological features** * absent ankle jerks/extensor plantars * cerebellar ataxia * optic atrophy * spinocerebellar tract degeneration **Other features** * hypertrophic obstructive cardiomyopathy (90%, most common cause of death) * diabetes mellitus (10-20%) * high-arched palate
25
Describe the classical history of vestibular schwannoma [4]
The classical history of vestibular schwannoma includes a combination of **vertigo, hearing loss, tinnitus and an absent corneal reflex.**
26
Describe the features of MS with regards to: - Vision [3] - Pain [4] - Muscles [3]
**Vision**: - 1 in 4 cases of MS present with **optic neuritis** : **temporary vision loss** (including a scotoma), **colour** **blindness** and **painful eye movements** - Examination may reveal **internuclear ophthalmoplegia** or a **pale optic disc on fundoscopy** **Pain**: * **Trigeminal** **neuralgia** * **Optic** **neuritis** * **Chest** **tightness** (or banding) * **Lhermitte**'s **phenomenon** **Muscle**: * **Spasticity** usually affects **legs** more than arms. * Can be associated with **spasms** that may **disturb sleep and lead to falls and issues with mobility** * Weakness usually affects **both lower limbs** > **one lower limb** > **upper and lower limb same side** > **an upper limb**
27
What may examination of eye reveal in a person presenting with ?optic neuritis in MS [2]
- Examination may reveal **internuclear ophthalmoplegia** or a **pale optic disc on fundoscopy**
28
Describe the presentation of optic neuritis [4] What is it specifically caused by? [1]
**presents** with **unilateral reduced vision**, developing over hours to days. **Key features are:** * **Central scotoma** (an enlarged central blind spot) * **Pain** with **eye** **movement** * **Impaired colour vision** * **Relative afferent pupillary defect** ## Footnote **NB**: **A relative afferent pupillary defect** is where the **pupil** in the **affected** eye **constricts** more **when shining a light in the contralateral eye** than when shining it in the affected eye. When testing the direct pupillary reflex, there is a reduced pupil response to shining light in the eye affected by optic neuritis. However, the affected eye has a normal pupil response when testing the consensual pupillary reflex.
29
Describe the pathophysiology and presentation of internuclear opthalmoplegia [+]
**Internuclear ophthalmoplegia** is caused by a **lesion** in the **medial longitudinal fasciculus**. The nerve fibres of the medial longitudinal fasciculus **connect the cranial nerve nuclei** (“**internuclear**”) that **control eye movements** (the **3rd, 4th and 6th cranial nerve nuclei**). These fibres are **responsible for coordinating the eye movements to ensure the eyes move together**. It causes **impaired adduction** on the **same side as the lesion** (the ipsilateral eye) and **nystagmus** in the **contralateral abducting eye**. **Basically** - If **right MLF** is **impacted**, the right eye cannot **adduct**. This means the left eye can still abduct, but it will have nystagmus - So if have right MLF lesion, when the right eye looks to the left it can't, so will look straight on. the left eye will abduct but have nystagmus - Right INO - has adduction deficit associated with horizontal nystagmus on contralateral side
30
Describe the disease modifying drugs used in MS [5+]
**natalizumab** * a recombinant monoclonal antibody that antagonises alpha-4 beta-1-integrin found on the surface of leucocytes * inhibit migration of leucocytes across the endothelium across the blood-brain barrier * generally considered to have the strongest evidence base for preventing relapse of the disease-modifying and hence is **often used first-line** * given intravenously **ocrelizumab** * humanized anti-CD20 monoclonal antibody * like natalizumab, it is considered a high-efficacy drug that is often used first-line * given intravenously **fingolimod** * sphingosine 1-phosphate (S1P) receptor modulator * prevents lymphocytes from leaving lymph nodes * oral formulations are available **beta-interferon** * not considered to be as effective as alternative disease-modifying drugs * given subcutaneously/intramuscularly **glatiramer acetate** * immunomodulating drug - acts as an 'immune decoy' * given subcutaneously * along with beta-interferon considered an 'older drug' with less effectiveness compared to monoclonal antibodies and S1P) receptor modulators
31
type IV hypersensitivity reaction
32
When taking a headache history, what are the key parts need to ask about?
**Onset and timing** * What was the patient doing at the time? (e.g. spontaneous or trauma) * How quickly did the headache reach maximum intensity? (e.g. within a few seconds or several days) * Has the headache been persistent since onset or come and go? **Location** **Unilateral**: - classic causes of a **unilateral headache include giant cell arteritis, migraine, or cluster headaches** **Bilateral**: - this may be **generalised or specific to a region such as a bilateral frontal headache in tension-type** - **Pain radiating from, or too, the neck and upper back** may indicate meningeal irritation seen in subarachnoid haemorrhage or meningitis. It may also be seen in cervical spondylosis. **Associated features** * **Nausea and/or vomiting**: commonly found in patients with migraine and form part of the diagnostic criteria. Also seen in patients with raised ICP (e.g. IIH, space-occupying lesion) and systemic illness (e.g. meningitis). * **Neck stiffness**: a cardinal feature of meningeal irritation and may indicate meningitis or subarachnoid haemorrhage. Neck pain may also occur in arterial dissection or cervical spondylosis. * **Photophobia**: this refers to a dislike for bright lights. A common feature of migraines and patients with meningeal irritation * **Phonophobia**: this refers to a dislike for loud sounds. Another common feature of migraines * **Visual changes:** changes can occur as part of an aura in migraine. Visual loss may occur in giant cell arteritis, acute angle-closure glaucoma or raised intracranial pressure. Cerebrovascular events or space-occupying lesions may affect the visual pathway leading to visual field defects. * **Focal neurological deficits:** this refers to neurological signs and symptoms that localised to a specific area such as left-sided weakness or a cranial nerve defect. The findings depend on the location of the abnormality. * **Global neurology deficits**: this refers to features consistent with global dysfunction of the brain. This is often due to raised intracranial pressure or severe infection. Features typically include altered mental status, seizures, and/or coma. **Past medical history** - Understanding a patients' co-morbidities are vital to determine the possible cause of headache. A really key question is whether the patient has **previously experienced headaches and how the current headache differs from those previous experiences.** Headache is always concerning in a patient with no previous history, especially in the elderly. Other parts of the medical history to think about include: * **Current or previous history of cancer:** may suggest metastatic spread * **Any trauma:** may indicate a bleed or fracture * **Any recent head and neck surgery:** could suggest a tracking infection or abscess * **Any thrombosis risk**: increased risk of cerebral venous thrombosis * **Drug history:** is there an element of medication overuse headache? * **Family history:** particularly around history of bleeding, subarachnoid haemorrhage or aneurysms
33
Describe the usual type of cluster headache patient [1]
A typical patient is a **30-50 year old male smoker**. They may have **triggers**, such as **alcohol, strong smells or exercise.**
34
Describe what is meant by Paroxysmal hemicrania (PH) [1] Describe the presentation [3]
**attacks** of **severe, unilateral headache, usually in the orbital, supraorbital or temporal region** - These attacks are often associated with **autonomic features**, usually last **less than 30 minutes** and can **occur multiple times a day.** (Occurring with frequency >5 times daily) **Either or both of the following:** **At least one of the following symptoms ipsilateral to the headache:** - conjunctival injection - lacrimation - nasal congestion - rhinorrhoea - eyelid oedema - forehead or facial sweating - miosis - ptosis. & **Restlessness or agitation**
35
How do you treat PH? [1]
PH is completely responsive to treatment with **indomethacin**. * **150mg of oral indomethacin daily** * This can be increased to **225mg daily if required**
36
How do you ddx PH from cluster headache? [4]
- PH **more** **frequent** but **lesser duration** - PH treated with **indomethacin** - PH does **not follow circadian rhythm** (time fo day) or circaannual rhythm (time of year) -PH **not associated to ptosis or miosis**
37
How would you Ix for PH? [1]
In any case of severe, unilateral headache, a diagnostic trial of indomethacin can be considered, sometimes referred to as an '**indotest'** - **a 50mg IM injection of indomethacin would be expected to give almost immediate protection from any further attacks for around 12 hours**
38
Describe the acute treatment for migraine [+]
**first-line**: **offer combination therapy with** * an **oral triptan and an NSAID**, or * an **oral triptan and paracetamol** * for young people aged 12-17 years consider a **nasal triptan in preference to an oral triptan** * if the above measures are not effective or not tolerated offer a **non-oral preparation of metoclopramide or prochlorperazine** and consider **adding a non-oral NSAID or triptan** In the UK, **new calcitonin gene-related peptide (CGRP) inhibitors** may be used in **acute migraine in patients who fail to respond to triptans or other standard treatments**, or that these treatments are not tolerated or contraindicated. - The main drug licensed for this indication is **Rimegepant**, which can be taken orally. - These medications **bind to the CGRP receptor** and **subsequently block attachment of CGRP** which is a potent vasodilator that can amplify and perpetuate migraine headache pain.
39
What is status migrainosus? [1]
: a **debilitating migraine that persists for longer than 72 hours.**
40
Describe what is meant by Foster kennedy syndrome [1]
**unilateral optic atrophy** (vision loss in one eye) and **contralateral papilledema** (swelling of the optic disc in the other eye), often caused by a space-occupying lesion in the brain compressing the optic nerve
41
A 12-year-old child developed headaches, vomiting and a staggering gait. A cerebellar neoplasm was diagnosed. Which is the most common cerebellar neoplasm of childhood? Ependymoma Glioblastoma multiforme Neuroblastoma Astrocytoma Oligodendroglioma
Astrocytoma
42
What is the histology like of a meningioma? [1]
* Histology: **Spindle cells in concentric whorls and calcified psammoma bodies**
43
State and explain the standard investigation for acromegaly? [1] Name two others [2]
**Insulin-like growth factor-1 (IGF-1):** can be tested on a blood sample. It indicates the growth hormone level and is raised in acromegaly. - **First line** **OGTT**: - Make patient fast - At time 0, check glucose and GH - Give 75g dose of glucose and wait 2hrs - Normal response: suppression of GH when glucose given - **Acromegaly response: GH increases despite glucose given** - Used to **confirm after IGF-1 tests** **MRI pituitary** | Testing growth hormone directly is unreliable: fluctuates in the day.
44
Name three drug therapies for acromegaly? [3]
**Octreotide** - somatostatin analogue: lowers GH levels / blocks GH release - **first line** **Pegvisomont** – GH receptor antagonist; subcutaneous injection **Bromocriptine** (Dopamine agonists): block growth hormone release
45
Management of Cushing's syndrome: - Surgery? [1] - Drugs? [2]
** Trans-sphenoidal surgery** Adrenolytics:  **Ketoconazole**: causes steroidogenesis inhibition.  **Metyrapone**: reduces the production of cortisol in the adrenals and is occasionally used in treating of Cushing’s
46
There are three types of dexamethason suppression test. Describe them [3]
**Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome**) - A **normal** result is that the **cortisol** level is **suppressed**. - **Failure** of the dexamethasone **to suppress the morning cortisol** could indicate **Cushing**’s **syndrome**, and further assessment is required. THINK CAPE **Low-dose 48-hour test (used in suspected Cushing’s syndrome)** - **0.5mg** is taken every **6 hours for 8 doses,** starting at **9 am on the first day**. - Cortisol is **checked at 9 am on day 1** (before the first dose) and **9 am on day 3** (after the last dose) - A **normal** result is that the **cortisol level on day 3 is suppressed** - Failure of the dexamethasone to suppress the **day 3 cortisol could indicate Cushing’s syndrome, and further assessment is required**. **High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)** - carried out the same way as the low-dose test, other than using **2mg per dose** (rather than 0.5mg). - This **higher dose is enough to suppress the cortisol in Cushing’s disease**, but **not when it is caused by an adrenal adenoma or ectopic ACTH.**
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51
How do you calculate CPP / cerebral perfusion pressure? [1] What is normal CPP? [1]
**CPP = MAP – ICP** - CPP normally **60-80 (150) mmHg**
52
Examination fndings of SAH? [4] ECG Changes? [2]
**fundoscopy**: - **subhyaloid haemorrhages** may be visible **meningeal signs**: positive Kernig's or Brudzinski's signs may be elicited **papilloedema**: though uncommon, may be present indicating raised intracranial pressure vital signs: **hypertension** is commonly observed; however, **hypotension** is a **poor** **prognostic** sign **ECG changes:** * **transient** ECG changes including **ST elevation** may be seen * this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
53
Ix for SAH? [3]
**non-contrast CT head** is the first-line investigation of choice - if **CT head is done within 6 hours of symptom onset** and is **normal**: consider an alternative diagnosis (DON'T do an LP) - if **CT head is done MORE than 6 hours** after symptom onset and is **normal**: **DO an LP** (should occur within 12hrs) **if the CT shows evidence of a SAH** * **referral** to **neurosurgery** to be made as soon as SAH is confirmed After **spontaneous SAH is confirmed**, the aim of investigation is to **identify a causative pathology** that needs urgent treatment: * **CT intracranial angiogram** (to identify a vascular lesion e.g. aneurysm or AVM) * **+/- digital subtraction angiogram (catheter angiogram)**
54
Complications of aneurysmal SAH? [5]
**re-bleeding** * happens in around 10% of cases and most common in the first 12 hours * if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged * associated with a high mortality (up to 70%) **hydrocephalus** * hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt **vasospasm** (also termed delayed cerebral ischaemia), typically 7-14 days after onset * ensure euvolaemia (normal blood volume) * consider treatment with a vasopressor if symptoms persist **hyponatraemia** (most typically due to syndrome inappropriate anti-diuretic hormone (**SIADH**)) **seizures**
55
Describe the current NICE guidelines on CT imaging for head trauma [+]
56
Head trauma comes to A&E. What would be an alarming sign and why?
**Unequal pupils** ---> Alarming sign , **indicates increased ICP & asymmetric mass effect.**
57
A patient with head trauma comes in with unequal pupils. What would be next immediate appropriate steps? [5]
**Measures to lower high ICP:** * **Head elevation** (30 degrees) * **Remove neck restrains** (unless unstable spine injury) * **Hyperventilation** (pCO2: 4-4.5 kpa) for **cerebral vasoconstriction** * **Mannitol, hypertonic saline**
58
How do you tx Cushing's triad? [
**Mannitol**, an osmotic diuretic medication, is often provided intravenously and can be highly effective in lowering ICP and increasing CPP **diuretics** (e.g., furosemide), **steroids** (e.g., methylprednisolone), and **sedatives** (e.g., propofol) Rarely, a **craniotomy**, or removal of a small portion of the skull, may be performed to alleviate the rising pressure.
59
State what type of herniation A-D are [4]
A: **Cingulate** (Subfalcine) B: **Central** (**transtentorial**) C: **Uncal** D: Downward cerebellar (**Tonsillar**)
60
What is normal ICP [1] Was can a ICP of greater than cause herniation? [1]
Normal adult **ICP: 5 - 15 mmHg** (supine position). A mass lesion with an ICP **of ≥ 20 mmHg can cause herniation.**