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Neuroscience Flashcards

1
Q

What is Bell’s palsy?

A

An acute, unilateral, idiopathic, facial nerve paralysis that fully evolves within 72 hours

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2
Q

What is the aetiology of Bell’s palsy?

A

Viral which is strongly associated with the herpes simplex virus (type 1)

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3
Q

What is the epidemiology of Bell’s palsy?

A

Peak incidence is 20-40 years
More common in pregnant women

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4
Q

What are the risk factors for Bell’s palsy?

A

Pregnancy (x3)
Diabetes (x5)

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5
Q

What are the features of Bell’s palsy?

A
  1. Lower motor neuron facial nerve palsy - forehead affected (in contrast, an UMN lesion ‘spares’ the upper face)
  2. Patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis
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6
Q

What are the investigations for Bell’s palsy?

A
  1. Clinical diagnosis: acute, unilateral facial palsy, with an otherwise normal physical examination
  2. Tests to rule out other causes e.g. Ramsay Hunt syndrome (VZV), CT for stroke or SOL
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7
Q

What are the causes of 7th nerve palsy?

A
  1. Bell’s palsy
  2. Ramsay Hunt syndrome
  3. Lyme disease
  4. Brainstem lesions: stroke, tumour, MS
  5. Cerebellopontine tumours: acoustic neuromas
  6. Systemic disease: DM, Guillain-Barre
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8
Q

What differentiates Lyme disease, Guillain–Barré, sarcoid, and trauma from Bell’s palsy?

A

They all often present with bilateral weakness

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9
Q

What is the management for Bell’s palsy?

A
  1. All patients should receive oral prednisolone within 72 hours of onset of Bell’s palsy
  2. Antiviral treatment in combination with a corticosteroid may be of small benefit, but seek specialist advice if this is being considered - NICE
  3. Eye care to prevent exposure keratopathy: prescription of artificial tears and eye lubricants and microporous tape for night if unable to close
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10
Q

What is the follow up for Bell’s palsy?

A
  1. If the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT
  2. Referral to plastic surgery may be appropriate for patients with more long-standing weakness e.g. several months
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11
Q

What is the prognosis for Bell’s palsy?

A

Most people with Bell’s palsy make a full recovery within 3-4 months
If untreated around 15% of patients have permanent moderate to severe weakness

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12
Q

What are central nervous system tumours?

A

Primary tumours arising from any of the brain tissue types

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13
Q

What is the most common type of brain tumour?

A

Metastatic brain cancer
Often multiple and not treatable with surgical intervention
Tumours that most commonly spread to the brain include:
- Lung (most common)
- Breast
- Bowel
- Skin (namely melanoma)
- Kidney

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14
Q

What is the most common primary brain tumour in adults?

A

Glioblastoma multiforme

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15
Q

What are the features of glioblastomas on imaging?

A
  1. Solid tumours with central necrosis and a rim that enhances with contrast
  2. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema
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16
Q

What are the histological features of glioblastomas?

A

Pleomorphic tumour cells border necrotic areas

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17
Q

What is the management and prognosis of glioblastomas?

A

Surgical with postoperative chemotherapy and/or radiotherapy Dexamethasone is used to treat the oedema
Prognosis is poor ~ 1 year

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18
Q

What are the second most common primary brain tumours?

A

Meningiomas

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19
Q

What are meningiomas?

A

Typically BENIGN, extrinsic tumours of the CNS
They arise from the arachnoid cap cells of the meninges and are typically located next to the dura
Cause symptoms by compression rather than invasion

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20
Q

What are the histological features of meningiomas?

A

Spindle cells in concentric whorls and calcified psammoma bodies

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21
Q

What is the management plan for a meningioma?

A

Investigation is with CT (will show contrast enhancement) and MRI
Treatment will involve either observation, radiotherapy or surgical resection

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22
Q

What is the most common primary brain tumour in children?

A

Astrocytomas

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23
Q

What are the common CNS tumours?

A

60% = Glioma and metastatic disease
20% = Meningioma
10% = Pituitary lesions

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24
Q

What are some of the common features of CNS tumours?

A
  1. Headache or vomiting (raised intracranial pressure)
  2. Epilepsy (focal or generalized)
  3. Focal neurological deficits (dysphagia, hemiparesis, ataxia, visual field defects, cognitive impairment)
  4. Personality change
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25
Q

How to symptoms of CNS tumours present depending on site of tumour?

A

Tumours arising in right temporal and frontal lobe may reach considerable size before becoming symptomatic
Whereas tumours in the speech and visual areas will typically produce early symptoms

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26
Q

What is the diagnostic investigation of choice for CNS tumours?

A

MRI scan - provide best resolution

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27
Q

What is the management plan for CNS tumours?

A
  1. Usually surgery - even if tumour cannot be completely resected conditions such as rising ICP can be addressed with tumour debulking → survival and quality of life prolonged
    1a. Curative surgery can usually be undertaken with lesions such as meningiomas
    1b. *Gliomas have a marked propensity to invade normal brain and resection of these lesions is nearly always incomplete (hence poor prognosis)
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28
Q

What are vestibular schwannomas?

A

Previously termed acoustic neuroma
Benign tumour arising from the eighth cranial nerve (vestibulocochlear nerve)
Often seen in the cerebellopontine angle
It presents with hearing loss, facial nerve palsy (due to compression of the nearby facial nerve) and tinnitus

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29
Q

What are bilateral vestibular schwannomas associated with?

A

Neurofibromatosis type 2

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30
Q

What are cluster headaches?

A
  1. An attack of severe pain localised to the UNILATERAL orbital/supra-orbital and/or temporal areas.
  2. Known to be one of the most painful conditions that patients can have the misfortune to suffer
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31
Q

What is the pattern of headaches in cluster headaches?

A

Typically occur in clusters lasting several weeks, with the clusters themselves typically once a year
Can last between 15 minutes to 3 hours

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32
Q

What is the epidemiology of cluster headaches?

A

More common in men (3:1) and smokers

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33
Q

What can trigger a cluster headache?

A

Alcohol

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34
Q

What are the features of cluster headaches?

A
  1. Intense sharp, stabbing pain around one eye (once or twice a day, each 15mins-2 hours), patient is restless and agitated during the attack
  2. Redness, lacrimation and lid swelling
  3. Nasal stuffiness
  4. May have mitosis and ptosis
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35
Q

How long do clusters typically last in cluster headaches?

A

4-12 weeks

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36
Q

What are the investigations for cluster headaches?

A

Neuroimaging: 1st line is MRI gadolinium
May find underlying brain lesions even if the clinical symptoms are typical for cluster headache

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37
Q

What is the management for cluster headaches?

A

NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches
1. Acute
2. Prophylaxis

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38
Q

What is the management for an acute cluster headache?

A
  1. 100% oxygen (80% response rate within 15 minutes)
  2. Subcutaneous triptan (75% response rate within 15 minutes)
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39
Q

What is the prophylaxis management for cluster headaches?

A
  1. Verapamil is the drug of choice
    (there is also some evidence to support a tapering dose of prednisolone)
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40
Q

What diseases are part of the trigeminal autonomic cephalgia group?

A
  1. Cluster headaches
  2. Paroxysmal hemicrania
  3. Short-lived unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)
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41
Q

What should happen to patients with a disease from the trigeminal autonomic cephalgia group?

A

Patients should be referred for specialist assessment as specific treatment may be required, e.g. paroxysmal hemicrania responds very well to indomethacin

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42
Q

What is encephalitis?

A

Inflammation of the brain parenchyma

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43
Q

What is the pathophysiology of encephalitis?

A
  1. HSV-1 is responsible for 95% of cases in adults
  2. Typically affects temporal and inferior frontal lobes
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44
Q

What are the features of encephalitis?

A
  1. Fever
  2. Headache
  3. Psychiatric symptoms (change in personality)
  4. Seizures
  5. Vomiting
  6. Focal features e.g. aphasia
    (peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis)
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45
Q

What are the signs of encephalitis on examination?

A

1.Reduced level of consciousness with deteriorating GCS
2. Seizures
3. Pyrexia
4. Signs of meningism: Neck stiffness, photophobia
5. Signs of raised ICP: hypertension, bradycardia, papilloedema.
6.Mini-mental examination may reveal cognitive or psychiatric disturbances

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46
Q

What are the investigations for encephalitis?

A
  1. Lumbar puncture: cerebrospinal fluid
    a. Lymphocytosis
    b. Elevated protein
    c. PCR for HSV, VZV and enteroviruses
  2. Neuroimaging:
    a. medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
    b. normal in one-third of patients
    c. MRI is better
  3. EEG: lateralised periodic discharges at 2 Hz
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47
Q

What is the management of encephalitis?

A

IV aciclovir should be started in all cases of suspected encephalitis

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48
Q

What is Kernigs sign in meningism?

A

Positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance)
Indicates the presence of meningitis or subarachnoid haemorrhage

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49
Q

What is epilepsy?

A

A common neurological condition characterised by recurrent seizures

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50
Q

Are there any associated diseases with epilepsy?

A

Most commonly occurs in isolation
Can be associated with:
1. Cerebral palsy - 30% have epilepsy
2. Tuberous sclerosis
3. Mitochondrial diseases

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51
Q

How are seizures in epilepsy classified?

A

3 key features:
1. Where seizures begin in the brain
2. Level of awareness during a seizure
3. Any other features of seizures

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52
Q

What are the two main types of epilepsy?

A

Focal seizures
Generalised seizures

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53
Q

What are focal seizures?

A
  1. Start in a specific area on one side of the brain
  2. Level of awareness can vary
  3. Can be further classified into motor (e.g. Jacksonian march) or non-motor (e.g. deja vu) or other such as aura
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54
Q

What are generalised seizures?

A
  1. These engage or involve networks on both sides of the brain at onset
  2. Consciousness is lost immediately (no level of awareness)
  3. Can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)
  4. Specific types: tonic-clonic, tonic, clonic, typical absence and myoclonic (brief rapid muscle jerks)
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55
Q

What is a focal to bilateral seizure?

A

Where the seizure starts on one side of the brain in a specific area before spreading to both lobes

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56
Q

What are some of the signs and features of epilepsy?

A
  1. Seizure activity: level of awareness, motor vs non-motor
  2. Biting their tongue
  3. Incontinence of urine
  4. Post-ictal phase: drowsy and tired for around 15 minutes
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57
Q

What are the features of a seizure originating in the temporal lobe?

A
  1. May occur with or without impairment of consciousness
  2. An aura occurs in most patients (e.g. rising epigastric sensation, deja vu, less commonly hallucinations)
  3. Seizures typically last around 1 minute
  4. Automatisms are common (e.g. lip smacking, grabbing, plucking)
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58
Q

What are the features of a seizure originating in the frontal lobe?

A
  1. Head/leg movements
  2. Posturing
  3. Post-ictal weakness
  4. Jacksonian march
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59
Q

What are the features of a seizure originating in the parietal lobe?

A

Paraesthesia

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60
Q

What are the features of a seizure originating in the occipital lobe?

A

Floaters/ flashes

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61
Q

What are the investigations for epilepsy?

A

For any seizure: A to E approach, including blood glucose to exclude hypoglycaemia, think cardiac causes too
Following their first seizures, patients generally have both an EEG and imaging = MRI

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62
Q

What is the management of epilepsy?

A
  1. Most neurologists start anti-epileptics following a SECOND epileptic seizure
  2. Common medications include sodium valproate (not for females of reproductive age), Carbamazepine, Lamotrigine, Phenytoin
  3. Other considerations include:
    a. DVLA
    b. Other medications (enzyme inducers and inhibitors to need to check)
    c. women wishing to get pregnant or on contraceptives (talk to specialist neurologist)
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63
Q

What are the DVLA rules for patients who have epilepsy?

A

Patients cannot drive for 6 months following a seizure
Must be fit free for 12 months before being able to drive

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64
Q

What are the common anti-epileptic drugs?

A
  1. Sodium valproate: used for generalised seizures in men, P450 inhibitor
  2. Carbamazepine: used second line for focal seizures, P450 induced, side effects include leucopenia and agranulocytosis, dizziness
    *3. Lamotrigine: used for a variety of generalised and focal seizures with a limited side effect profile (other than Stevens-Johnson syndrome)
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65
Q

What is the acute management of seizures?

A
  1. Most seizures terminate spontaneously
  2. If they don’t after 5-10 minutes: appropriate to administer ‘rescue’ medication = benzodiazepines such as diazepam (intranasally or buccal midazolam)
  3. If a patient continues to fit despite such measures = status epilepticus = MEDICAL EMERGENCY
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66
Q

What is status epilepticus?

A

Either:
1. A single seizure lasting > 5 mins or
2. More than 2 seizures within a 5 minute period without the person turning normal between them
MEDICAL EMERGENCY

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67
Q

What is the priority in status epilepticus?

A

Termination of seizure activity, which if prolonged will lead to irreversible brain damage

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68
Q

What is the management of status epilepticus?

A
  1. ABC: airway adjunct, oxygen, check blood glucose
  2. First line medication = IV benzodiazepines e.g. diazepam or lorazepam - this can be repeated after 10-20 minutes
  3. If ongoing (or established) status, it is appropriate to start a second line agent e.g. phenytoin or phenobarbital infusion
  4. If no response (refractory status) within 45 minutes from onset = general anaesthesia (best way to achieve rapid control of seizure activity)
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69
Q

What are the complications of epilepsy?

A
  1. Fractures with tonic-clonic seizures
  2. Sudden death in epilepsy
  3. Side effects of AEDs e.g. neutropenia, osteoporosis with carbamazepine
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70
Q

What is an extradural haemorrhage?

A

A bleed between the dura mater and the inner surface of the skull

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71
Q

What is the difference between an extradural haemorrhage and a haematoma?

A

A haematoma is a collection of blood and a haemorrhage is an acute bleed (most commonly becomes a haematoma)

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72
Q

What is the aetiology of an extradural haematoma?

A

Almost always caused by trauma and most typically ‘low impact trauma’
E.g. a blow to the head or a fall
The affected artery = middle meningeal artery: thin skill at the pterion overlies this and is vulnerable to injury
Collection of blood is therefore in the temporal region

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73
Q

What are the features of an extradural haematoma?

A
  1. Patient initially loses, briefly regains and then loses consciousness again after a low-impact head injury
  2. As the haematoma expands: patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibres of the third CN
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74
Q

What is the brief regain in consciousness in an extradural haemorrhage known as?

A

The lucid interval
Consciousness is lost again due to the expanding haematoma and brain hernia
As the haematoma expands the uncut of the temporal love herniates = compression of parasympathetic fibres of CN3

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75
Q

What is the investigation of choice for an extradural haematoma?

A

Non-contrast CT
Shows a biconvex (or lentiform), hyperdense collection around the surface of the brain
Looks like a lemon
Collection is limited by the suture lines of the skull

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76
Q

What is the management for an extradural haematoma?

A
  1. In patients with no neurological deficit: cautious clinical and radiological observation may be appropriate
  2. Definitive treatment: craniotomy and evacuation of the haematoma (if midline shift and brain stem herniate - needs early surgical intervention)
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77
Q

What is Guillain-Barre syndrome?

A

An immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)

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78
Q

What is the infection commonly associated with Guillain-Barre syndrome?

A

Campylobacter jejuni

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79
Q

What is the pathophysiology of Guillain-Barre syndrome?

A
  1. An inflammatory process
  2. Cross-reaction of antibodies after a recent infection which reacts with self-antigen on myelin on neurons
  3. Correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features, found in 25% of patients
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80
Q

What is Miller Fisher syndrome?

A

A variant of Guillain-Barre syndrome
Associated with:
1. Ophthalmoplegia
2. Areflexia
3. Ataxia
Eye muscles are typically affected first
Usually presents as a descending paralysis rather than ascending (opposite to Guillain-Barre)

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81
Q

What are the characteristic features of Guillain-Barre syndrome?

A
  1. Initially may experience back/leg pain
  2. Later develop progressive, symmetrical weakness of all the limbs
    2a. Weakness is ASCENDING (legs are affected first)
    2b. Reflexes are reduced or absent
  3. Sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs
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82
Q

What are some of the other features of Guillain-Barre syndrome?

A
  1. Progressive, symmetrical ascending weakness of all the limbs
  2. May be a history of gastroenteritis
  3. Respiratory muscle weakness
  4. Cranial nerve involvement:
    a. Diplopia
    b. Bilateral facial nerve palsy
    c. Oropharyngeal weakness
  5. Autonomic involvement:
    a. Urinary retention
    b. Diarrhoea
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83
Q

What is a less common finding in Guillain-Barre syndrome?

A

Papilloedema
Thought to be secondary to reduced CSF resorption

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84
Q

What are the investigations of Guillain-Barre syndrome?

A
  1. Lumbar puncture:
    Rise in protein with a normal WCC = (albuminocytologic dissociation)
  2. Nerve conduction studies:
    a. Decreased motor nerve velocity due to demyelination
    b. Prolonged distal motor latency
    c. Increased F wave latency
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85
Q

What is a severe sign of Guillain-Barre syndrome on examination?

A

Type 2 respiratory failure
Important to identify early e.g. CO2 retention flap, bounding pulse, drowsiness
Can be insidious and needs regular assessment

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86
Q

What is the management and prognosis of Guillain-Barre syndrome?

A

Medical management:
1. IVIG
2. Plasma exchange (plasmapheresis)
MDT approach: Physiotherapy, SALT, Occupational therapy
Prognosis:
Takes between 6-12 months for full recovery in strength, can take as long as three years

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87
Q

What is Horner’s syndrome?

A

A disorder characterised by:
1. Miosis (small pupil)
2. Ptosis (dropping of the upper eyelid)
3. Anhidrosis (loss of sweating on one side)
Plus enophthalmos = sunken eye

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88
Q

What is the aetiology of Horner’s syndrome?

A

Disruption of the sympathetic trunk supplying the eye

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89
Q

What are some of the causes of Horner’s syndrome?

A
  1. Carotid artery disscetion
  2. Tumour: in the neck or chest cavity e.g. Pancoast tumour in the upper part of the lung
  3. Lesion in the midbrain, brainstem, upper spinal cord or eye
  4. inflammation affecting the lymph nodes of the neck
  5. Surgery or trauma to the neck or spinal cord
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90
Q

What are the features of Horner’s syndrome?

A

Unilateral symptoms
1. Miosis
2. Ptosis
3. Anhidrosis
(plus enophthalmos = sunken eye)

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91
Q

How can congenital and acquired Horner’s syndrome be distinguished?

A

Congenital = present since birth
Heterochromia (difference in eye colour) is seen in congenital Horner’s

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92
Q

How can anhidrosis in Horner’s syndrome distinguish where the lesion is?

A
  1. Anhidrosis of the face, arm and trunk = central lesion (S)
    a. Stroke
    b. Syringomyelia
    c. MS
    d. Tumour
    e. Encephalitis
  2. Anhidrosis of the face = pre-ganglionic lesion (T)
    a. Pancoast tumour
    b. Thyroidectomy
    c. Trauma
    d. Cervical rib
  3. No anhidrosis = post-ganglionic lesion (C)
    a. Carotid artery dissection
    b. Carotid aneurysm
    c. Cavernous sinus thrombosis
    d. Cluster headache
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93
Q

What are the investigations for Horner’s syndrome?

A
  1. Drops e.g. aproclonidine: will cause significant dilation of the healthy eye and little dilation of the affected eye if Horner syndrome is caused by a third-order neuron abnormality — a disruption somewhere in the neck or above
  2. Imaging: e.g. CXR for Pancoast tumour, MRI/ CT for tumour in brain/ neck, Carotid USS for dissection
  3. Bloods: inflammatory markers
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94
Q

What is the management for Horner’s syndrome?

A

Often resolves when the underlying cause is treated e.g. surgery, chemotherapy/ radiotherapy for tumours

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95
Q

What is Huntington’s disease?

A

An inherited autosomal dominant neurodegenerative condition, which is progressive and incurable

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96
Q

What is Huntington disease characterised by?

A

Progressive chorea and dementia
Typically commencing in middle age

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97
Q

What is the pathophysiology of Huntington’s disease?

A
  1. Autosomal dominant
  2. Trinucleotide repeat disorder: repeat expansion of CAG
  3. Results in degeneration of cholinergic and GABA-ergic neurons in the striatum of the basal ganglia
  4. Due to a defect in huntingtin gene on Chr 4
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98
Q

What is anticipation in the context of Huntington’s disease?

A

It is a trinucleotide repeat disorder
Phenomenon of anticipation where the disease presents at an earlier age in successive generations

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99
Q

What are the features of Huntington’s disease?

A

Typically develop after 35 years
1. Chorea (involuntary, jerky dyskinetic movements)
2. Personality changes (e.g. irritability, apathy, depression) and intellectual impairment
3. Dystonia (spasms)
4. Saccadic eye movements (quick simultaneous movement of both eyes)
5. May develop cognitive deficits a.k.a dementia

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100
Q

What are the investigations for Huntington’s disease?

A
  1. Genetic analysis: diagnostic if >39 CAG repeats in the HD gene
  2. Imaging:
    a. Brain MRI or CT may show symmetrical atrophy of the striatum (particularly the caudate nuclei) and butterfly dilation of the lateral ventricles
    b. not specific as it is seen in other conditions
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101
Q

What is the management for Huntington’s disease?

A

Incurable
Treatment for dystonia and depression .e.g. haloperidol
Occupational therapy have a large role

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102
Q

What is the prognosis of Huntington’s disease?

A

Typically results in death 20 years after the initial symptoms develop

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103
Q

What is Ramsay Hunt syndrome?

A

A syndrome caused by the reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve (facial nerve)

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104
Q

What are the features of Ramsay Hunt syndrome?

A
  1. Auricular pain (often the first feature)
  2. Facial nerve palsy
  3. Vesicular rash around the ear
  4. Other features include vertigo and tinnitus
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105
Q

What is the management of Ramsay Hunt syndrome?

A

Oral aciclovir and corticosteroids

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106
Q

What is hydrocephalus?

A

A condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain
Caused by an imbalance between CSF production and absorption

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107
Q

How can hydrocephalus be broadly divided?

A

Obstructive ‘non-communicating’ and non-obstructive ‘communicating’

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108
Q

What is obstructive hydrocephalus caused by?

A
  1. Due to a structural pathology blocking the flow of CSF
  2. Dilation of the ventricular system is seen superior to the site of obstruction
  3. Causes include tumours, acute haemorrhage e.g. SAH or intraventricular and developmental abnormalities e.g. aqueduct stenosis
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109
Q

What is non-obstructive hydrocephalus caused by?

A
  1. Imbalance of CSF production or absorption
  2. Either caused by an increased production of CSF e.g choroid plexus tumour (very rare)
  3. More commonly caused by a failure of reabsorption at the arachnoid granulations e.g. meningitis or post-haemorrhagic stroke
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110
Q

What is normal pressure hydrocephalus?

A
  1. A unique form of non-obstructive hydrocephalus
  2. Characterised by large ventricles but normal ICP
  3. Classic triad of symptoms:
    a. Dementia
    b. Incontinence
    c. Disturbed gait
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111
Q

What are the features of hydrocephalus?

A
  1. Patients usually present with symptoms of raised ICP
  2. Headaches: typically worse in the morning, when lying down and during valsalva (forceful expiration against a closed airway)
  3. Nausea and vomiting
  4. Papilloedema
  5. Coma in severe cases
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112
Q

What are the investigations for hydrocephalus?

A

1st line: CT head: fast and shows adequate resolution of the brain and ventricles
2. MRI may be helpful for further detail especially if there is an underlying lesion
3. Lumbar puncture:
a. Both diagnostic and therapeutic in non-obstructive hydrocephalus
b. Allows sampling of CSF, measuring the opening pressure
c. Also allows drainage of CSF to reduce the pressure

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113
Q

When must you NOT carry out a lumbar puncture in hydrocephalus?

A

LP must not be used in obstructive hydrocephalus = the drainage of CSF will cause a difference in cranial and spinal pressures leading to brain herniation (coning)

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114
Q

What is the management of hydrocephalus?

A
  1. External ventricular drain: used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  2. Ventriculoperitoneal shunt: long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum
  3. In obstructive hydrocephalus: may involve treating the obstructive pathology e.g tumour, SAH
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115
Q

What is the epidemiology of hydrocephalus?

A

Bimodal age distribution:
1. In the young = congenital malformations and tumours
2. in the elderly = tumours and strokes

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116
Q

What is idiopathic intracranial hypertension?

A

A condition classically seen in young, overweight females with features of headache, blurred vision and papilloedema

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117
Q

What are the risk factors for idiopathic intracranial hypertension?

A
  1. Obesity
  2. Female sex
  3. Pregnancy
  4. Drugs: COCP, steroids, tetracyclines, retinoids, lithium
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118
Q

What are the features of idiopathic intracranial hypertension?

A
  1. Headache
  2. Blurred vision
  3. Papilloedema
  4. Enlarged blind spot
  5. Sixth nerve palsy (abducens)
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119
Q

What is 6th nerve palsy?

A

The most common ocular motor paralysis to occur in isolation in adults
The eye cannot abduct (due to lack of innervation of the lateral rectus)

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120
Q

What is the management of idiopathic intracranial hypertension?

A
  1. Weight loss
  2. Diuretics e.g. acetazolamide
  3. Topiramate - added benefits of causing weight loss
  4. Repeated LP may be a temporary measure
  5. Surgery:
    a) optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve
    b) lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce ICP
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121
Q

What is an intracranial venous thrombosis?

A

A thrombosis that can cause cerebral infarction
50% of patients have isolated sagittal sinus thromboses
50% have coexistent lateral sinus thromboses and cavernous sinus thromboses

122
Q

What is a sagittal sinus thrombosis?

A
  1. May present with seizures and hemiplegia
  2. Parasagittal biparietal or bifrontal haemorrhages
  3. Empty delta sign seen on venography
123
Q

What is a cavernous sinus thrombosis?

A
  1. Causes: local infection e.g. sinusitis, neoplasia, trauma
  2. Periorbital oedema
  3. Ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
  4. Trigeminal nerve involvement: hyperaesthesia of upper face and eye pain
  5. Associated with central retinal vein thrombosis
124
Q

What is a lumbar puncture?

A

When a spinous tap is inserted between two vertebrae to remove a sample of CSF

125
Q

What are the indications for a lumbar puncture?

A
  1. Diagnostic: infections e.g. meningitis, hydrocephalus
  2. Injection: painkillers, spinal anaesthetic (epidural)
  3. Therapeutic: removal of CSF to reduce ICP or pressure on spine
126
Q

What are the complications of a lumbar puncture?

A

Side effects are uncommon
1. Headaches
2. Swelling and lower back pain where the needle was inserted
3. Infection/ bleeding at site of injection
4. Always check patients medication for anti-coagulants

127
Q

What is a post-LP headache?

A
  1. Headache following LP
  2. Occurs in 1/3rd of patients
128
Q

What is the pathophysiology of post-LP headaches?

A

Unclear- may related to ‘leak’ of CSF following dural puncture

129
Q

What is the epidemiology of post-LP headaches?

A

More common in young females with a low BMI

130
Q

What are the features of a post-LP headache?

A
  1. Usually develops within 24-48 hours following LP (can be as late as 1 week later)
  2. May last several days
  3. Worsens with upright position
  4. Improves with recumbent position
131
Q

What are some of the factors that may contribute to post-LP headache?

A
  1. Increased needle size
  2. Direction of bevel
  3. Not replacing the stylet
  4. Increased number of LP attempts
132
Q

What is the management of post-LP headaches?

A
  1. Supportive initially e.g. analgesia, rest
  2. If pain > 72 hours then specific treatment may be needed to prevent subdural haematoma
  3. Options include: blood patch, epidural saline and IV caffeine
133
Q

What is meningitis?

A

Inflammation of the meninges commonly caused by infection

134
Q

What are the common causative organisms for meningitis in 0-3 months old?

A
  1. Group B strep
  2. E.coli
  3. Listeria monocytogenes
135
Q

What are the common causative organisms for meningitis in 3 months -6 years old?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae
136
Q

What are the common causative organisms for meningitis in 6-60 years old?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
137
Q

What are the common causative organisms for meningitis in the >60s?

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis
  3. Listeria monocytogenes
138
Q

What is the most common causative organism for meningitis in the immunosuppressed?

A

Listeria monocytogenes

139
Q

What are the symptoms of meningitis?

A
  1. Headache
  2. Fever
  3. Nausea/ vomiting
  4. Photophobia
  5. Drowsiness
  6. Seizures
140
Q

What are the signs of meningitis on physical examination?

A
  1. Neck stiffness
  2. Purpuric rash (particularly with invasive meningococcal disease)
141
Q

What are the investigations for meningitis?

A

All patients should be transferred to hospital for urgent treatment
1. ABC approach: including blood cultures
2. Senior review if there are any warning signs present
3. Lumbar puncture to confirm diagnosis (however should be delayed if there are certain circumstances e.g. signs of ICP)

142
Q

What are the warning signs in meningitis?

A
  1. Rapidly progressive rash
  2. Poor peripheral perfusion
  3. RR < 8 or > 30 / min or pulse rate < 40 or > 140 / min
  4. pH < 7.3 or WBC< 4 *109/L or lactate > 4 mmol/L
  5. GCS < 12 or a drop of 2 points
  6. Poor response to fluid resuscitation
143
Q

What are the circumstances in which you would delay a lumbar puncture in meningitis?

A
  1. Signs of severe sepsis or a rapidly evolving rash
  2. Severe respiratory/cardiac compromise
  3. Significant bleeding risk
  4. Signs of raised intracranial pressure:
    a. focal neurological signs
    b. papilloedema
    c. continuous or uncontrolled seizures
    d. GCS ≤ 12
144
Q

What are the CSF findings for bacterial meningitis?

A
  1. Cloudy appearance
  2. Low glucose (<1/2 plasma)
  3. High protein (>1g/L)
  4. 10-5,000 polymorph WCC
145
Q

What are the CSF findings for viral meningitis?

A
  1. Clear (maybe cloudy) appearance
  2. Normal glucose (60-80% of plasma glucose)
  3. Normal/ raised protein
  4. 15-1,000 lymphocytes
146
Q

What are the CSF findings for TB meningitis?

A
  1. Slightly cloudy appearance with a fibrin web
  2. Low glucose (< 1/2 plasma)
  3. High protein (>1g/L)
  4. 30-300 lymphocytes (not as raised as bacterial, which is also polymorphic)
147
Q

What are the CSF findings for fungal meningitis?

A
  1. Cloudy appearance
  2. Low glucose
  3. High protein
  4. 20-200 lymphocytes
148
Q

What additional test is used for suspected bacterial meningitis?

A

PCR, sensitivity of 75%
(Ziehl-Neelsen stain is only 20% sensitive)

149
Q

What is the management for meningitis (without indication for delayed LP)?

A
  1. IV access: take blood and cultures
  2. LP: if not within first hour, give IV antibiotics after blood cultures have been taken
  3. IV antibiotics
  4. IV dexamethasone as an adjunct (but avoid in septic shock, meningococcal septicaemia or if immunocompromised)
  5. CT scan is not normally indicated
150
Q

What are the IV antibiotic guidelines for bacterial meningitis?

A

3 months - 50 years: cefotaxime or cefrtriaxone
> 50 years: cefotaxime (or ceftriaxone) PLUS amoxicillin (or ampicillin) for adults (cover Listeria)

151
Q

What is the management of meningitis in patients with signs of raised ICP?

A
  1. Get critical care input
  2. Secure airway and give high flow oxygen
  3. IV access: take bloods and blood culture
  4. Give IV dexamethasone and IV antibiotics
  5. Arrange neuroimaging
152
Q

What is the management of meningitis in patients with signs of severe sepsis or a rapidly evolving rash?

A

Get critical care input
Sepsis 6 pathway:
1. Administer high flow oxygen
2. Take blood cultures
3. Give antibiotics: cefotaxime (or ceftriaxone) ± amoxicillin (depends on age)
4. Give IV fluid (bolus of 500ml crystalloid over less than 15 minutes)
5. Measure serum lactate
6. Measure hourly urine output

153
Q

What are the other additional investigations for meningitis?

A
  1. Bloods: FBC, renal function, glucose, lactate
  2. VBG/ ABG (depending on how ill the patient is)
  3. If LP has been performed: microscopy and culture, glucose and protein of CSF, PCR and HSV/ VZV
  4. Consider throat swab for meningococcal culture
154
Q

What is the management of contacts in meningococcal meningitis?

A

Prophylaxis needs to be offered to households and close contacts of patients affected with meningococcal meningitis if they were in close contact 7 days before onset
Oral ciprofloxacin or rifampicin may be used
Meningococcal vaccination should be offered

155
Q

What are the causes of viral meningitis?

A
  1. Non-polio enteroviruses e.g. coxsackie virus, echovirus
  2. Mumps
  3. Herpes simplex virus (HSV), cytomegalovirus (CMV), herpes zoster viruses
  4. HIV
  5. Measles
156
Q

What are the risk factors for viral meningitis?

A
  1. Patients at the extremes of age (< 5 years and the elderly)
  2. Immunocompromised, e.g. patients with renal failure, with DM
  3. Intravenous drug users
157
Q

What is the epidemiology of viral meningitis?

A

Much more common than bacterial meningitis and more benign
Patients do not often present to medical services

158
Q

What are the common features of viral meningitis?

A
  1. Headache
  2. Evidence of neck stiffness
  3. Photophobia (often milder than in in bacterial meningitis)
  4. Confusion
  5. Fevers
159
Q

What are the less common features of viral meningitis?

A
  1. Focal neurological deficits on examination
  2. Seizures: suggest meningoencephalitis
160
Q

What are the investigations for viral meningitis?

A
  1. LP: normal glucose, normal/ raised protein
  2. PCR for organism
161
Q

What is the management for viral meningitis?

A
  1. Supportive whilst awaiting results of LP
  2. If any suggestion of bacterial meningitis or encephalitis then treatment should be started (cefotaxime/ cefrtriaxone or aciclovir respectively)
  3. Aciclovir may be used if the patient has meningitis secondary to HSV
162
Q

What is the prognosis of viral meningitis?

A

Self-limiting
Symptoms should improve over the course of 7-14 days
Complications are rare in immunocompetent patients

163
Q

What is the difference between a primary and secondary headache?

A

A primary headache has no underlying cause e.g. migraine, cluster headache, tension-type

164
Q

What are the red flags for a headache?

A
  1. Vomiting without other obvious cause
  2. Worsening headache with fever
  3. Sudden onset ‘thunderclap’
  4. New-onset neurological deficit
  5. New onset cognitive dysfunction
  6. Change in personality
  7. Impaired level of consciousness
  8. Recent head trauma
  9. Orthostatic headache
  10. A substantial change in the characteristics of their headache
165
Q

What is a migraine?

A

A common type of primary headache

166
Q

What are the characteristic features of a migraine?

A
  1. A severe, unilateral throbbing headache
  2. Associated with naeuae, photophobia and photophobia
  3. Attacks may last up to 72 hours
  4. Attacks may be precipitated by an aura
167
Q

What are the typical auras in a migraine?

A

Visual, progressive and are characterised by transient hemianopia disturbance or a spreading scintillating scotoma

168
Q

How long can a migraine ‘attack’ last for?

A

Up to 72 hours

169
Q

What is the epidemiology of migraines?

A

3 times more common in women
M = 6%, F = 18%

170
Q

What are some common triggers for a migraine attack?

A
  1. Tiredness, stress
  2. Alcohol
  3. COCP
  4. Lack of food or dehydration
  5. Foods: cheese, chocolate, red wines, citrus fruits
  6. Menstruation
  7. Bright lights
171
Q

What is the migraine diagnostic criteria?

A

A- at least 5 attacks fulfilling criteria B-D
B - headaches lasting 4-72 hrs
C- Has at least 2 of the following:
1. Unilateral location
2. Pulsating quality (varying with the heartbeat)
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity
D- During headache at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and photophobia
E - not attributed to another disorder

172
Q

What is a hemiplegic migraine?

A

A variant of migraine in which motor weakness is a manifestation of aura in some attacks
50% of patients have a strong FH
Very rare

173
Q

What are some differentials for a migraine?

A

Exclude infectious cause e.g. meningitis
Exclude SAH
Rule out red flags for a SOL
Idiopathic intracranial hypertension - offer fundoscopy for papilloedema

174
Q

What are the investigations for migraines?

A

Usually clinical using the diagnostic criteria
Must be at least 5 attacks which fulfilled the criteria

175
Q

What is the management for migraines?

A

Divided into acute and prophylaxis treatment
Acute: 5-HT receptor agonists
Prophylaxis: 5-HT receptor antagonists

176
Q

What is the acute treatment for migraines?

A

1st line: combination of oral triptan and an NSAID/ paracetamol
1a. For young people consider nasal triptan > oral
2. If the above measures are not effective, offer a non-oral preparation of metoclopramide or prochlorperazine and cosnider adding a non-rap NSAID or triptan

177
Q

What is the prophylaxis treatment of migraines?

A

Should be given if patients are experiencing 2 or more attacks per month
1. Topiramate or propranolol (depending on patient preference, comorbidities and risk of adverse events)
2. In women of childbearing age: propranolol > topiramate (can be teratogenic and reduce effectiveness of hormonal contraceptives)
3. Riboflavin may be effective, 400mg once daily
4. For women with predictable menstrual migraine = frovatriptan (2.5 mg twice a day) or zolmitriptan (2.5 mg twice or three times a day) as a type of ‘mini-prophylaxis’

178
Q

What is an important caution of using metoclopramide in the acute management of migraines?

A

Young patients can develop acute dystonic reactions from it

179
Q

What are the considerations of migraines and the COCP?

A

If patients experience a migraine with aura then the COCP is absolutely contraindicated due to an increased risk of stroke

180
Q

What is recommended for women who experience migraines around the time of menstruation?

A

Can be treated with mefanamic acid or a combination of aspirin, paracetamol and caffeine
Triptans are also recommended in the acute situation

181
Q

What are the considerations of using HRT in a patient who experiences migraines?

A

It is safe to prescribe however this may make the migraines worse

182
Q

What are the complications of migraines?

A
  1. Disruption of daily activities
  2. Can progress into analgesia-overuse headaches due to chronic use of analgesia
  3. Gastric ulcers from overuse of NSAIDs
183
Q

What is motor neuron disease?

A

A neurological condition of unknown cause
Can present with both upper and lower motor neurone signs
Has various patterns of disease

184
Q

What are the different pattern of diseases in motor neuron disease?

A
  1. Amyotrophic lateral sclerosis
  2. Progressive muscular atrophy
  3. Bulbar palsy
185
Q

What are some of the features of motor neuron disease?

A
  1. Fasciculations
  2. The absence of sensory symptoms/ signs
  3. The mixture of lower motor neuron and upper motor neuron signs
  4. Wasting of the small hand muscles/ tibialis anterior
186
Q

What are some of the other features of motor neuron disease?

A

(classic mixture of UMN and LMN signs, plus absence of sensory signs)
1. Does not affect the external ocular muscles
2. No cerebellar signs
3. Abdominal reflexes are usually preserved
4. Sphincter dysfunction if present is a late feature

187
Q

What are the UMN and LMN signs in motor neuron disease?

A

LMN:
1. Muscle wasting
2. Fasciculations
3. Flaccid weakness
4. Depressed or absent reflexes
UMN:
1. Spastic weakness
2. Brisk reflexes
3. Extensor plantars (Babinski reflex)

188
Q

What are the investigations for motor neuron disease?

A

Clinical diagnosis
Investigations can confirm by providing evidence of UMN and LMN:
1. Bloods: creatinine kinase would be elevated, ESR
2. EMG: acute and chronic denervation, reduced number of action potentials with increased amplitude
3. Nerve conduction studies: most often normal
4. MRI: to exclude cord compression and myelopathy

189
Q

What age does motor neuron disease start to present?

A

Rarely presents before 40

190
Q

What is Amyotrophic lateral sclerosis?

A

A type of motor neuron disease (50% of patients have ALS)
1. typically LMN signs in arms and UMN signs in legs
2. in familial cases the gene responsible lies on chromosome 21

191
Q

What is Primary lateral sclerosis?

A

UMN signs only

192
Q

What is Progressive muscular atrophy?

A

Type of motor neuron disease
1. LMN signs only
2. Affects distal muscles before proximal
3. Carries best prognosis

193
Q

What is Progressive bulbar palsy?

A

Type of motor neuron disease
1. Palsy of the tongue, muscles of chewing/swallowing and facial muscles 2. Due to loss of function of brainstem motor nuclei
3. Carries worst prognosis

194
Q

What is the management of motor neuron disease?

A
  1. Riluzole: prevents stimulations of glutamate receptors and prolongs life by about 3 months, used mainly for ALS
  2. Respiratory care: non-invasive ventilation (BIPAP) used at night, improves survival by around 7 months
  3. Nutrition: PEG (percutaneous gastrostomy tube) is the preferred way to support nutrition and prolongs survival
195
Q

What is the prognosis of motor neuron disease?

A

Poor prognosis
50% of patients die within 3 years

196
Q

What is multiple sclerosis?

A

A chronic cell-mediated autoimmune disorder characterised by demyelination in the central nervous system

197
Q

What is the epidemiology of multiple sclerosis?

A
  1. 3 times more common in women
  2. Most commonly diagnosed in people aged 20-40 years
  3. Much more common at higher latitudes
198
Q

What is essential for the diagnosis of multiple sclerosis?

A

Demonstration of two or more relapses and clinical evidence of two or more lesions disseminated in time and space

199
Q

What are the three main subtypes of multiple sclerosis?

A
  1. Relapsing-remitting (most common)
  2. Secondary progressive disease
  3. Primary progressive disease
200
Q

What is relapsing and remitting multiple sclerosis?

A
  1. Most common form of MS (85%)
  2. Acute attacks which last 1-2 months
  3. These are followed by periods of remission
201
Q

What is secondary progressive disease in multiple sclerosis?

A
  1. Relapsing-remitting patients who have deteriorated and developed neurological signs between relapses
  2. 65% of patients with relapsing-remitting disease will develop this within 15 years of diagnosis
  3. Gait and bladder disorders are seen
202
Q

What is primary progressive disease in multiple sclerosis?

A
  1. Accounts for 10% of patients
  2. Progressive deterioration from onset
  3. More common in older people
203
Q

What are the main features of multiple sclerosis?

A
  1. Non-specific symptoms e.g. significant lethargy
  2. Optic neuritis (most common presenting feature)
  3. Sensory symptoms e.g. pins/needles, numbness, trigeminal neuralgia
  4. Motor: spastic weakness, most commonly in legs
  5. Cerebellar signs: ataxia (in acute relapse), tremor
  6. Others: urinary incontinence, sexual dysfunction, intellectual deterioration
204
Q

What is the common presenting feature in multiple sclerosis?

A

Optic neuritis:
1. Unilateral decrease in visual acuity over hours or days
2. Pain worse on eye movement
3. Relative afferent pupillary defect
4. Central scotoma (blind spot)

205
Q

What are the causes of optic neuritis?

A
  1. Multiple sclerosis (most common)
  2. Diabetes
  3. Syphilis
206
Q

What are the features of optic neuritis?

A
  1. Unilateral decrease in visual acuity over hours or days
  2. Poor discrimination of colours
  3. Pain worse on eye movement
  4. Relative afferent pupillary defect
  5. Central scotoma (blind spot)
207
Q

What is the investigation for optic neuritis?

A

MRI of the brain and orbits with gadolinium contrast

208
Q

What is the management for optic neuritis?

A

High dose steroids- recovery usually takes 4-6 weeks

209
Q

What is the prognosis for optic neuritis?

A

On MRI: if >3 white matter lesions, the 5-year risk of developing multiple sclerosis is 50%

210
Q

What are the visual features of multiple sclerosis?

A
  1. Optic neuritis
  2. Optic atrophy
  3. Uhthoff’s phenomenon: worsening of vision following rise in body temperature
  4. Internuclear ophthalmoplegia
211
Q

What are the sensory features of multiple sclerosis?

A
  1. Pins/ needles
  2. Numbness
  3. Trigeminal neuralgia
  4. Lhermitte’s syndrome: paraesthesia in limbs on neck flexion
212
Q

What is the motor feature on multiple sclerosis?

A

Spastic weakness which is most commonly seen in the legs

213
Q

What are the cerebellar features of multiple sclerosis?

A
  1. Ataxia: more often seen in an acute relapse
  2. Tremor
214
Q

What are some of the non-neurological features of multiple sclerosis?

A
  1. Urinary incontinence
  2. Sexual dysfunction
  3. Intellectual deterioration
215
Q

How is the diagnosis of multiple sclerosis made?

A

Imaging and CSF analysis
Requires demonstration of lesions disseminated in time and space

216
Q

What are the MRI findings of multiple sclerosis?

A
  1. High signal T2 lesions
  2. Periventricular plaques
  3. Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum
217
Q

What are the CSF findings of multiple sclerosis?

A
  1. Oligoclonal bands (and not in serum)
  2. Increased intrathecal synthesis of IgG
218
Q

What are the visual evoked potentials for multiple sclerosis?

A

Delayed but well preserved waveform

219
Q

What is the aim of management of multiple sclerosis?

A

Focused on reducing the frequency and duration of relapses

220
Q

What is the management of an acute relapse of multiple sclerosis?

A
  1. High dose steroids e.g. oral or IV methylprednisolone may be given for 5 days
  2. Steroids shorten the duration of the relapse but do not alter the degree of recovery (i.e. whether the patient returns to their baseline)
221
Q

What are the indications for using disease modifying drugs in the management of multiple sclerosis?

A

Aim: reduce risk of relapse
1. relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
2. secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

222
Q

What are the different disease modifying drugs for multiple sclerosis?

A
  1. Natalizumab: IV, recombinant monoclonal antibody (first line for preventing relapses)
  2. Orelizumab: IV, anti-CD20 monoclonal antibody
  3. Fingolimod: oral
  4. Beta-interferon: not as effective, S/C
  5. Glatiremer acetate: immune decoy, given S/C
223
Q

How can fatigue be managed in multiple sclerosis?

A

Once other problems (e.g. anaemia, thyroid or depression) can be excluded, a trial of amantadine can be started
Other options include mindfulness and CBT

224
Q

How can spasticity be managed in multiple sclerosis?

A
  1. Baclofen and gabapentin are first line
  2. Other options: diazepam, dantrolene and tizanidine
  3. Physiotherapy is important
225
Q

How can bladder dysfunction be managed in multiple sclerosis?

A
  1. May take the form of urgency, incontinence or overflow
  2. Ultrasound first: assess bladder emptying as anticholinergics may worsen symptoms
    2a. If significant residual volume = intermittent self-catherisation
    2b. If no significant residual volume = anticholinergics may improve urinary frequency
226
Q

How can oscillopsia (visual fields appear to oscillate) be managed in multiple sclerosis?

A

First line is gabapentin

227
Q

What is myasthenia gravis?

A

An autoimmune disorder resulting in insufficient functioning acetylcholine receptors
Antibodies to acetylcholine receptors are seen in 85-90% of cases

228
Q

What is the epidemiology of myasthenia gravis?

A

Twice as common in women (2:1)

229
Q

What is the key feature is myasthenia gravis?

A

Muscle fatiguability:
Muscles become progressively weaker during periods of activity and slowly improve after periods of rest

230
Q

What are the features of myasthenia gravis?

A

Muscle fatiguability:
1. Extraocular muscle weakness = diplopia
2. Proximal muscle weakness = face, neck, limb girdle
3. Ptosis
4. Dysphagia

231
Q

What are the associated diseases in myasthenia gravis?

A
  1. Thymomas (15%)
  2. Autoimmune disorders: pernicious anaemia, autoimmune thyroid diseases, rheumatoid arthritis, SLE
  3. Thymic hyperplasia in 50-70%
232
Q

What are the investigations for myasthenia gravis?

A
  1. Single fibre electromyography: high sensitivity
  2. CT thorax to exclude thymoma
  3. Antibodies to acetylcholine receptors: positive in 85-90%
  4. In remaining patients, offer anti-muscle specific tyrosine kinase antibodies
  5. Normal creatinine kinase
  6. Tensilon test: not commonly used due to risk of cardiac arrhythmia
233
Q

What is the management of myasthenia gravis?

A
  1. Long acting acetylcholinesterase inhibitors = pyridostigmine
  2. Immunosuppression (not started at diagnosis) = prednisolone, azathioprine, cyclosporine, mycophenolate mofetil
  3. Thymectomy (if thymoma)
234
Q

What is a myasthenic crisis?

A

Life-threatening exacerbation of myasthenia gravis / weakness requiring intubation or non-invasive ventilation

235
Q

What is the most common exacerbating factor in myasthenia gravis?

A

Exertion

236
Q

What drugs can exacerbate myasthenia gravis?

A
  1. Penicillamine (used in Wilson’s disease)
  2. Beta blockers
  3. Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
  4. Lithium
  5. Phenytoin
237
Q

What is the management of myasthenic crisis?

A
  1. Plasmapharesis
  2. IV immunoglobulins
238
Q

What is Neurofibromatosis?

A

An autosomal dominant genetic disorder affecting cells of neural crest origin, resulting in the development of multiple neurocutaneous tumours

239
Q

What are the two types of neurofibromatosis?

A
  1. Type 1 (more common than type 2):
    a. Café-au-lait spots (>= 6, 15 mm in diameter)
    b. Axillary/groin freckles
    c. Peripheral neurofibromas
    d. Iris hamatomas (Lisch nodules) in > 90%
    e. Scoliosis
    f. Pheochromocytomas
    Type 2:
    a. Bilateral vestibular schwannomas
    b. Multiple intracranial schwannomas, mengiomas and ependymomas
240
Q

What are the presenting symptoms of Neurofibromatosis?

A
  1. Type 1 NF:
    a. Skin lesions (cafe au lait spots)
    b. Learning difficulties (in 40%)
    c. Headaches
    d. Disturbed vision (optic gliomas, in 15%)
    e. Precocious puberty (may indicate lesions of the pituitary from optic glioma involving the chiasm)
  2. Type 2 NF:
    a. Hearing loss
    b. Tinnitus
    c. Balance problems
    d. Headache
    e. Facial pain
    f. Numbness
241
Q

What is the aetiology of Neurofibromatosis?

A

Autosomal dominant so there may be a family history, but 50% are caused by new mutations

242
Q

What are the investigations for Neurofibromatosis?

A
  1. Ophthalmological assessment and audiometry
  2. MRI brain and spinal cord: For vestibular schwannomas, meningiomas and nerve root neurofibromas, other brain tumours, hydrocephalus
  3. Skull X-ray: Sphenoid dysplasia in type 1 NF
  4. Genetic testing: identifiable mutation involving the NF1 locus and NF2
243
Q

What is Parkinson’s disease?

A

A progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra

244
Q

What is the triad of symptoms in Parkinson’s disease?

A
  1. Bradykinesia
  2. Tremor
  3. Rigidity
    (symptoms are often asymmetrical)
245
Q

What is the aetiology of Parkinson’s disease?

A
  1. Sporadic and idiopathic (most common): Unknown
  2. Environmental toxins and oxidative stress have been proposed (e.g. pesticides, wood pulp)
  3. Secondary:
    a. Neuroleptic therapy (e.g. in schizophrenia)
    b. Vascular insults (e.g. basal ganglia or midbrain strokes)
    c. Repeated head injury (e.g. boxing)
246
Q

What is the epidemiology of Parkinson’s disease?

A
  1. Around twice as common in men
  2. Mean age of diagnosis is 65 years
247
Q

What are the main features of Parkinson’s disease?

A
  1. Bradykinesia:
    a. poverty of movement also seen, sometimes referred to as hypokinesia
    b. short, shuffling steps with reduced arm swinging
    c. difficulty in initiating movement
  2. Tremor:
    a. most marked at rest, 3-5 Hz
    b. worse when stressed or tired, improves with voluntary movement
    c. typically ‘pill-rolling’, i.e. in the thumb and index finger
  3. Rigidity:
    a. lead pipe
    b. cogwheel: due to superimposed tremor
248
Q

What are the other features of Parkinson’s disease?

A
  1. Mask-like face
  2. Flexed posture
  3. Micrographia
  4. Drooling of saliva
  5. Psychiatric features:
    a. depression is the most common feature (affects about 40%)
    b. dementia, psychosis and sleep disturbances may also occur
  6. Impaired olfaction
  7. REM sleep behaviour disorder: fatigue
  8. Autonomic dysfunction:
    postural hypotension
249
Q

How is Parkinson’s disease investigated?

A
  1. Diagnosis is usually clinical
  2. Levodopa trial:
    a. Timed walking and clinical assessment after levodopa may be informative
  3. Bloods: Exclude other causes, serum ceruloplasmin (excludes Wilson’s disease in young onset)
  4. CT or MRI brain: Useful for excluding other causes of gait decline (e.g. hydrocephalus, vascular disease)
  5. If there is difficulty differentiating between essential tremor and Parkinson’s disease: NICE recommend considering 123I‑FP‑CIT single photon emission computed tomography (SPECT)
250
Q

What are the features of drug-induced Parkinsonism?

A
  1. Motor symptoms are generally rapid onset and bilateral
  2. Rigidity and rest tremor are uncommon
251
Q

What is the general management of Parkinson’s disease?

A
  1. If the motor symptoms are affecting the patient’s quality of life: levodopa
  2. If the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor
252
Q

What is the benefit of Levodopa in the management of Parkinson’s disease compared to Dopamine agonists and MAO-B inhibitors?

A
  1. More improvement in motor symptoms
  2. More improvement in activities of daily living
253
Q

What is the next step of management if a patient continues to have symptoms despite optimal levodopa treatment or has developed dyskinesia?

A

NICE recommend the addition of a dopamine agonist, MAO‑B inhibitor or catechol‑O‑methyl transferase (COMT) inhibitor as an adjunct

254
Q

What are the common adverse effects of Levodopa?

A
  1. Dry mouth
  2. Anorexia
  3. Palpitations
  4. Postural hypotension
  5. Psychosis
  6. Dyskinesias at peak dose: dystonia, chorea and athetosis (involuntary writhing movements)
  7. Important to not acutely stop Levodopa
255
Q

What are the common adverse effects of Levodopa?

A
  1. Dry mouth
  2. Anorexia
  3. Palpitations
  4. Postural hypotension
  5. Psychosis
  6. Dyskinesias at peak dose: dystonia, chorea and athetosis (involuntary writhing movements)
  7. Important to not acutely stop Levodopa
256
Q

What is the risk of Parkinson’s disease treatment if medication is not taken/absorbed (e.g. due to gastroenteritis)?

A

Risk of acute akinesia or neuroleptic malignant syndrome

257
Q

What medication for acute confusional state should be avoided in patient’s with Parkinson’s disease?

A

Haloperidol (0.5 mg is usually the first-line sedative): makes Parkinsonism worse
Give benzodiazepine or atypical antipsychotics: quetiapine and clozapine

258
Q

What is raised intracranial pressure?

A
  1. As the brain and ventricles are enclosed by a rigid skull, they have a limited ability to accommodate additional volume
  2. Additional volume (e.g. haematoma, tumour, excessive CSF) will therefore lead to a rise in intracranial pressure
  3. Its development may be acute or chronic
259
Q

What is the pathophysiology of raised ICP?

A
  1. The normal ICP is 7-15 mmHg in adults in the supine position
  2. Cerebral perfusion pressure (CPP) is the net pressure gradient causing cerebral blood flow to the brain
  3. CPP = mean arterial pressure - ICP
260
Q

What are the causes of raised ICP?

A
  1. Idiopathic intracranial hypertension
  2. Traumatic head injuries
  3. Infection: meningitis
  4. Tumours
  5. Hydrocephalus
261
Q

What are the features of raised ICP?

A
  1. Headache
  2. Vomiting
  3. Reduced levels of consciousness
  4. Papilloedema
  5. Cushing’s triad:
    a. widening pulse pressure
    b. bradycardia
    c. irregular breathing
262
Q

What is the key investigation for raised ICP?

A

CT/MRI of Head

263
Q

What other investigations can be used in raised ICP?

A

Invasive ICP monitoring:
1. Catheter placed into the lateral ventricles of the brain to monitor the pressure
2. May also be used to take collect CSF samples and also to drain small amounts of CSF to reduce the pressure
3. A cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP

264
Q

What is the management of raised ICP?

A
  1. Investigate and treat the underlying cause
  2. Head elevation to 30º
  3. IV mannitol may be used as an osmotic diuretic
  4. Controlled hyperventilation:
    a. aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
    b. leads to rapid, temporary lowering of ICP
  5. Removal of CSF, different techniques include:
    a. Drain from intraventricular monitor
    b. Repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
    c. Ventriculoperitoneal shunt (for hydrocephalus)
265
Q

What are the three characteristic features of raised intracranial pressure?

A

Headache
Papilloedema
Vomiting

266
Q

What is radiculopathy?

A
  1. A range of symptoms produced by the pinching of a nerve root in the spinal column
  2. Symptoms vary by location but frequently include pain, weakness, numbness and tingling
  3. Can be caused by narrowing of the space where nerve roots exit the spine, which can be a result of stenosis, bone spurs, disc herniation
267
Q

What are the symptoms of a prolapsed lumbar disc?

A
  1. Produces clear dermatomal leg pain associated with neurological deficits
  2. Leg pain usually worse than back
  3. Pain often worse when sitting
268
Q

What are features of a prolapsed lumbar disc according to the level of compression?

A
  1. L3 nerve root compression:
    a. Sensory loss over anterior thigh
    b. Weak hip flexion, knee extension and hip adduction
    c. Reduced knee reflex
    d. Positive femoral stretch test
  2. L4 nerve root compression:
    a. Sensory loss anterior aspect of knee and medial malleolus
    b. Weak knee extension and hip adduction
    c. Reduced knee reflex
    d. Positive femoral stretch test
  3. L5 nerve root compression: a. Sensory loss dorsum of foot
    b. Weakness in foot and big toe dorsiflexion
    c. Reflexes intact
    d. Positive sciatic nerve stretch test
  4. S1 nerve root compression:
    a. Sensory loss posterolateral aspect of leg and lateral aspect of foot
    b. Weakness in plantar flexion of foot
    c. Reduced ankle reflex
    d. Positive sciatic nerve stretch test
269
Q

What is the management of a prolapsed lumbar disc?

A
  1. Similar to that of other musculoskeletal lower back:
    a. pain: analgesia
    b. physiotherapy, exercises
  2. NICE recommend using the same drugs as for back pain without sciatica symptoms i.e. first-line is NSAIDs +/- proton pump inhibitors rather than using neuropathic analgesia (e.g. duloxetine)
  3. If symptoms persist e.g. after 4-6 weeks) then referral for consideration of MRI is appropriate
270
Q

What is the first line treatment for back pain?

A

NSAIDs (plus PPI if > 45)

271
Q

When should an MRI be offered to patients with back pain?

A

Should only be offered to patients with non-specific back pain ‘only if the result is likely to change management’ and to patients where malignancy, infection, fracture, cauda equina or ankylosing spondylitis is suspected

272
Q

Alongside NSAIDs, what is the management of non-specific back pain?

A
  1. Try to encourage self-management
  2. Stay physically active and exercise
273
Q

What is a Subdural haemorrhage?

A
  1. Acollection of blood deep to the dural layer of the meninges
  2. The blood is not within the substance of the brain and is therefore called an ‘extra-axial’ or ‘extrinsic’ lesion
  3. They can be unilateral or bilateral
274
Q

How can subdural haemorrhages be classified?

A

Acute
Subacute
Chronic

275
Q

What is the aetiology of a Subdural haemorrhage?

A

The primary aetiology of both acute and chronic subdural haematomas is trauma: results in shearing forces which tear veins (bridging veins) that travel from the dura to the cortex

276
Q

What is the epidemiology of Subdural haemorrhages?

A
  1. Acute:
    a. Tend to occur in younger patients/associated with major trauma (5–25% of cases of severe head injury)
    b. More common than extradural haemorrhage
  2. Chronic: More common in elderly
277
Q

What is an acute subdural haemorrhage?

A
  1. A collection of fresh blood within the subdural space and is most commonly caused by high-impact trauma
  2. Presentation ranges from an incidental finding in trauma to severe coma and coning due to herniation
278
Q

What is the first line investigation for acute subdural haemorrhage?

A

CT Head:
1. Will show a crescentic collection, not limited by suture lines
2. They will appear hyperdense (bright) in comparison to the brain
3. Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation

279
Q

What is the management of acute subdural haemorrhage?

A
  1. Small or incidental acute subdurals can be observed conservatively
  2. Surgical options include monitoring of intracranial pressure and decompressive craniectomy
280
Q

What is a subacute subdural haemorrhage?

A

Worsening headaches 7–14 days after injury, altered mental status

281
Q

What is a chronic subdural haematoma?

A

A collection of blood within the subdural space that has been present for weeks to months

282
Q

Who is at increased risk of chronic subdural haematomas?

A
  1. Elderly and alcoholic patients
  2. They have brain atrophy and therefore fragile or taut bridging veins which can rupture easily
283
Q

What are the presenting symptoms of chronic subdural haematomas?

A

Typically a several week to month progressive history of either confusion, reduced consciousness or neurological deficit:
a. Cognitive impairment
b. Psychiatric symptoms
c. Gait deterioration
d. Focal weakness
e. Seizures
(May not be a history of a fall in elderly/ alcoholics)

284
Q

What are the findings of a chronic subdural haematomas on CT imaging?

A
  1. Similarly are crescentic in shape, not restricted by suture lines and compress the brain (‘mass effect’)
  2. In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain
285
Q

What is the management of chronic subdural haematomas?

A
  1. If the chronic subdural is an incidental finding or if it is small in size with no associated neurological deficit then it can be managed conservatively with the hope that it will dissolve with time
  2. If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required
286
Q

What are the differences between an extradural and subdural haematoma?

A
  1. Extradural:
    a. Majority occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery
    b. Features of raised intracranial pressure
    c. Lucid interval
  2. Subdural:
    a. Bleeding into the outermost meningeal layer, around the frontal and parietal lobes
    b. Risk factors include old age, alcoholism and anticoagulation: risk of rupture of bridging veins
    c. May be fluctuating confusion/consciousness
287
Q

What is the prognosis for a Subdural haemorrhage?

A
  1. Acute: Underlying brain injury is the most important factor on outcome
  2. Chronic: Generally have a better outcome than acute SDHs, reflecting lower incidence of underlying brain injury, with good outcomes in 3/4 of those treated by surgery
288
Q

What is a Tension Headache?

A
  1. Form of episodic primary headache
  2. Often described as a ‘tight band’ around the head or a pressure sensation
  3. Symptoms tend to be bilateral (as opposed to migraine)
289
Q

What is the aetiology of a Tension Headache?

A
  1. Psychological stress is the most common trigger
  2. Other associated factors:
    a. Disturbed sleep patterns can result in episodic tension headaches
    b. Insomnia and other sleep disorders can result in chronic tension headaches
290
Q

What is the epidemiology of Tension Headaches?

A
  1. Probably the most common type of headache
  2. Most common between the ages of 20 to 39 years and then decline
  3. Patients either do not need treatment or they successfully self-treat and are therefore less likely to mention these headaches than patients with migraine
291
Q

What are the features of Tension Headaches?

A
  1. Often described as a ‘tight band’ around the head or a pressure sensation
  2. Symptoms tend to be bilateral
  3. Tends to be of a lower intensity than migraine
  4. Not associated with aura, nausea/vomiting or aggravated by routine physical activity
  5. May be related to stress
  6. May co-exist with migraine
292
Q

What is a Chronic tension-type headache?

A

A tension headache that occurs on 15 or more days per month

293
Q

What is the management of Tension Headaches?

A
  1. Acute treatment: aspirin, paracetamol or an NSAID are first-line
  2. Prophylaxis: NICE recommend ‘up to 10 sessions of acupuncture over 5-8 weeks’
294
Q

What are the complications of Tension Headaches?

A

Peptic ulcer: occurs secondary to NSAID use

295
Q

What is Trigeminal Neuralgia?

A
  1. A facial pain syndrome in the distribution of ≥1 divisions of the trigeminal nerve
  2. Characterised by severe unilateral pain
296
Q

What is the aetiology of Trigeminal Neuralgia?

A
  1. Majority of patients (80-90%): trigeminal nerve compression
  2. Other causes include: demyelinating disease such as MS
297
Q

What are the characteristics of Trigeminal Neuralgia?

A
  1. A unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
  2. The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously
  3. Small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
  4. The pain usually remits for variable periods
298
Q

What are the red flag symptoms and signs of Trigeminal Neuralgia that suggest a a serious underlying cause?

A
  1. Sensory changes
  2. Deafness or other ear problems
  3. History of skin or oral lesions that could spread perineurally
  4. Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  5. Optic neuritis
  6. A family history of MS
  7. Age of onset before 40 years
299
Q

What is the management of Trigeminal Neuralgia?

A
  1. Carbamazepine is first-line
  2. Failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
300
Q

What are the first line treatments for other causes of neuropathic pain e.g. diabetic neuropathy?

A
  1. Amitriptyline, duloxetine, gabapentin or pregabalin
  2. If the first-line drug treatment does not work try one of the other 3 drugs
301
Q

What are the palliative drugs?

A
  1. Secretions: hyoscine hydrobromide (glycopyrronium bromide can also be used)
  2. Agitation and confusion: haloperidol (terminal stage: midazolam)
  3. Intractable hiccups: chlorpromazine
  4. Pain: opioids, oxycodone is preferred to morphine if renal impairment
  5. Nausea and vomiting: dopamine antagonist (e.g. metoclopramide) or match cause of patient’s N+V

!Final Year (26 decks)

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