Neuro Flashcards

1
Q

Causes of bitemporal hemianopia?

A

caused by a lesion of optic chiasm

  1. upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
  2. lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
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2
Q

what is GBS?

A

Guillain-Barré syndrome is an “acute paralytic polyneuropathy” that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms. It is usually triggered by an infection and is particularly associated with to campylobacter jejuni, cytomegalovirus and Epstein-Barr virus.

it is an acute inflammatory demyelinating polyneuropathy

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3
Q

pathophys of guillain barre syndrome

A

Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon

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4
Q

presentation of GBS

A

Symmetrical ascending weakness (starting at the feet and moving up the body)
Reduced reflexes
There may be peripheral loss of sensation or neuropathic pain
It may progress to the cranial nerves and cause facial nerve weakness
there may also be autonomic dysfunction: sweating, raised pulse, BP changes, arrhythmias

proximal muscles are more affected (trunk, respiratory and cranial nerves - eps VII)

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5
Q

clinical course of GBS

A

Symptoms usually start within 4 weeks of the preceding infection. The symptoms typically start in the feet and progresses upward. Symptoms peak within 2-4 weeks, then there is a recovery period that can last months to years.

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6
Q

how is GBS diagnosed

A

A diagnosis of Guillain-Barré syndrome is made clinically. The Brighton criteria can be used for diagnosis.

Diagnosis can be supported by investigations:
Nerve conduction studies (reduced signal through the nerves)
Lumbar puncture for CSF (raised protein with a normal cell count and glucose)

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7
Q

management of GBS

A

IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis (pulmonary embolism is a leading cause of death)
4 hrly FVC measurement

In severe cases with impending respiratory failure, patients may need intubation, ventilation and admission to the intensive care unit.

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8
Q

prognosis for GBS

A

80% will fully recover
15% will be left with some neurological disability
5% will die

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9
Q

ddx for headaches

A

Tension headaches
Migraines
Cluster headaches
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Subarachnoid haemorrhage
Analgesic headache
Hormonal headache
Cervical spondylosis
Trigeminal neuralgia
Raised intracranial pressure (brain tumours)
Meningitis
Encephalitis

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10
Q

red flags in someone with a headache

A

Fever, photophobia or neck stiffness (meningitis or encephalitis)
New neurological symptoms (haemorrhage, malignancy or stroke)
Dizziness (stroke)
unilateral, eye pain and Visual disturbance (temporal arteritis or glaucoma)
Sudden onset worst headache, thunderclap (subarachnoid haemorrhage)
Worse on coughing or straining (raised intracranial pressure)
Postural, worse on standing, lying, in the morning or bending over (raised intracranial pressure)
Severe enough to wake the patient from sleep
Vomiting (raised intracranial pressure or carbon monoxide poisoning)
History of trauma (intracranial haemorrhage)
Pregnancy (pre-eclampsia)

persisting headache_/- scalp tenderness in over 50s - GCA

change in pattern of usual headaches

reduced lvl of consciousness

recent travel (malaria)

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11
Q

what examination is an important part of assessing a headache?

A

Fundoscopy examination to look for papilloedema is an important part of an assessment of a headache. Papilloedema indicates raised intracranial pressure, which may be due to a brain tumour, benign intracranial hypertension or an intracranial bleed.

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12
Q

tension headaches are associated with

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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13
Q

mx of tension type headaches

A

Reassurance
Basic analgesia
Relaxation techniques
Hot towels to local area

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14
Q

secondary headaches causes

A

Secondary headaches give a similar presentation to a tension headache but with a clear cause. They produce a non-specific headache secondary to:

Underlying medical conditions such as infection, obstructive sleep apnoea or pre-eclampsia
Alcohol
Head injury
Carbon monoxide poisoning

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15
Q

sinusitis headahces?

A

Sinusitis causes a headache associated with inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses. This usually produces facial pain behind the nose, forehead and eyes. There is often tenderness over the affected sinus, which helps to establish the diagnosis.

Sinusitis usually resolves within 2-3 weeks. Most sinusitis is viral. Nasal irrigation with saline can be helpful. Prolonged symptoms can be treated with steroid nasal spray. Antibiotics are occasionally required.

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16
Q

Analgesic Headache

A

An analgesic headache is a headache caused by long term analgesia use. It gives similar non-specific features to a tension headache. They are secondary to continuous or excessive use of analgesia. Withdrawal of analgesia important in treating the headache, although this can be challenging in patients with long term pain and those that believe the analgesia is necessary to treat the headache.

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17
Q

Hormonal Headache

A

Hormonal headaches are related to oestrogen. The produce a generic, non-specific, tension-like headache. They tend to be related to low oestrogen:

Two days before and first three days of the menstrual period
Around the menopause
Pregnancy. It is worse in the first few weeks and improves in the last 6 months. Headaches in the second half of pregnancy should prompt investigation for pre-eclampsia.

The oral contraceptive pill can improve hormonal headaches.

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18
Q

Cervical Spondylosis headache?

A

Cervical spondylosis is a common condition caused by degenerative changes in the cervical spine. It causes neck pain, usually made worse by movement. However, if often presents with headache.

it is important to exclude other causes of neck pain such as inflammation, malignancy and infection. It is also important to exclude spinal cord or nerve root lesions.

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19
Q

trigeminal neuralgia?

A

Trigeminal neuralgia can affect any combination of the branches of the trigeminal (V) nerve. 90% of cases are unilateral, 10% are bilateral. Around 5-10% of people with multiple sclerosis have trigeminal neuralgia.

It presents with intense facial pain that comes on spontaneously and last anywhere between a few seconds to hours. It is often described as an electricity-like shooting pain. attacks can be triggered by washing affected area, shaving, eating, talking, dental prostheses. Attacks often worsen over time.

secondary causes: compression of trigeminal root by anomalous or aneurysmal intracranial vessels or tumor, chronic meningeal inflammation, MS, zoster, skull base malformation. MRI is req to exclude 2ndary causes.

Tx - carbamazepine usually 1st line

other options - lamotrigine, phenytoin, gabapentin and surgery

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20
Q

Mx of trigeminal neuralgia

A

NICE recommend carbamazepine as first-line for trigeminal neuralgia. Surgery to decompress or intentionally damage the trigeminal nerve is an option.

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21
Q

diff types of migraines

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

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22
Q

typical migraine headahce presentation

A

more common in females

associated with obesity and fhx

Headaches last between 4 and 72 hours. Typical features are:
Moderate to severe intensity
Pounding or throbbing in nature
Usually unilateral but can be bilateral
photophobia
phonophobia
With or without aura (lasting 15-30 mins followed by headache within 1 hr)
Nausea and vomiting

Aura -
Aura is the term used to describe the sensorymotor changes associated with migraines. There can be multiple different types of aura:
visual -

Sparks in vision
Blurring vision
Lines across vision
Loss of different visual fields

somatosensory - paraesthesia

motor - dysarthria and ataxia. hemiparesis, ophthalmoplegia

speech - dysphasia or paraphasia

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23
Q

symptoms of hemiplegic migraine and initial management of someone presenting with symptoms of a hemiplegic migraine

A

Symptoms of a hemiplegic migraine can vary significantly. They can be of sudden or gradual onset and can include:
Typical migraine symptoms
Hemiplegia (unilateral weakness of the limbs)
Ataxia
Changes in consciousness

Hemiplegic migraines can mimic stroke. It is essential to act fast and exclude a stroke in patients presenting with symptoms of hemiplegic migraine.

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24
Q

triggers for migraine

A
  • Stress
  • Bright lights
  • Strong smells
  • Certain foods (e.g. chocolate, cheese and caffeine)
  • Dehydration
  • Menstruation
  • oral contraceptives
  • Abnormal sleep patterns
  • Trauma
  • alcohol
  • travel
    • exercise
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25
Q

5 stages of a migraine

A

These stages are not typical of everyone and they will vary between patients. Some patients may only experience one or two of the stages. The prodromal stage can involve several days of subtle symptoms such as yawning, fatigue or mood changes prior to the onset of the migraine.

  • Premonitory or prodromal stage (can begin 3 days before the headache)
  • Aura (lasting up to 60 minutes)
  • Headache stage (lasts 4-72 hours)
  • Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)
    • Postdromal or recovery phase
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26
Q

acute mx of migraine

A

Often patients will go to a dark quiet room and sleep. Options for medical management are:

  • Paracetamol
  • oral Triptans (e.g. sumatriptan 50mg as the migraine starts)
  • NSAIDs (e.g ibuprofen or naproxen)
    • Antiemetics if vomiting occurs (e.g. metoclopramide)
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27
Q

triptans? and CIs

A

They are 5HT receptors agonists (serotonin receptor agonists)

Triptans are used to abort migraines when they start to develop

They act on:

  • Smooth muscle in arteries to cause vasoconstriction
  • Peripheral pain receptors to inhibit activation of pain receptors
    • Reduce neuronal activity in the central nervous system

CI - IHD, coronary spasm, uncontrolled hypertension, recent lithium, SSRIs, ergot use

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28
Q

Migraine Prophylaxis

A

headache diary - identify and then avoid the triggers, also useful in demonstrating the response to treatment.

  • Propranolol
  • Topiramate (this is teratogenic and can cause a cleft lip/palate so patients should not get pregnant)
  • Amitriptyline

Acupuncture is an option recommended by NICE recommend for the treatment of migraines. It is reported to be as effective as prophylactic medications.

Supplementation with vitamin B2 (riboflavin) may reduce frequency and severity.

In migraine specifically triggered around menstruation, prophylaxis with NSAIDs (e.g. mefanamic acid) or triptans (frovatriptan or zolmitriptan) can be used as a preventative measure.

botulinum injections are a last resort

Migraines tend to get better over time and people often go into remission from their symptoms.

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29
Q

cluster headaches presentation

A

they come in clusters of attacks and then disappear for a while. For example, a patient may suffer 3 – 4 attacks a day for 4-12 weeks followed by a pain-free period lasting months to 1-2 years. Attacks last between 15 minutes and 3 hours. it can be chronic as well rather than episodic.

more common in males and smokers.

Attacks can be triggered by things like alcohol, strong smells and exercise.

Cluster headaches are often described as one of the most severe and intolerable pains in the world. They are sometimes referred to as “suicide headaches” due to the severity of the pain.

Symptoms are typically all unilateral:

  • Red, swollen and watering eye (lacrimation)
  • Pupil constriction (miosis)
  • Eyelid drooping (ptosis)
  • Nasal discharge (rhinorrhoea)
  • Facial sweating (flushing)
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30
Q

treatment options for cluster headahces

A

Acute management:

  • Triptans (e.g. sumatriptan injected subcutaneously)
  • High flow 100% oxygen for 15-20 minutes via non-rebreathable maks(can be given at home)

Prophylaxis options:

  • avoid triggers eg alcohol
  • Verapamil
  • Lithium
    • corticosteroids such as prednisolone (a short course ONLY for 2-3 weeks to break the cycle during clusters)
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31
Q

RFs for intracranial bleeds

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
    • Anticoagulants such as warfarin
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32
Q

presentation of intracranial haemorrhage

A

Sudden onset headache is a key feature. They can also present with:

  • Seizures
  • Weakness
  • Vomiting
  • Reduced consciousness
  • Other sudden onset neurological symptoms
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33
Q

presentation of intracranial bleeding

A

Sudden onset headache is a key feature. They can also present with:

  • Seizures
  • Weakness
  • Vomiting
  • Reduced consciousness
  • Other sudden onset neurological symptoms
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34
Q

below which GCS score do u need to consider securing someone’s airway

A

When someone has a score of 8 or below then you need to consider securing their airway as there is a risk they are not able to maintaining it on their own.

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35
Q

what are the components of GCS

A

GCS is used to assess level of consciousness

Eyes

  • Spontaneous = 4
  • Speech = 3
  • Pain = 2
  • None = 1

Verbal response

  • Orientated = 5
  • Confused conversation = 4
  • Inappropriate words = 3
  • Incomprehensible sounds = 2
  • None = 1

Motor response

  • Obeys commands = 6
  • Localises pain = 5
  • Normal flexion = 4
  • Abnormal flexion = 3
  • Extends = 2
    • None = 1
36
Q

subdural haemorrhage

A

Subdural haemorrhage is caused by rupture of the bridging veins in the outermost meningeal layer. They occur between the dura mater and arachnoid mater. On a CT scan they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).

Subdural haemorrhages occur more frequently in elderly or alcoholic patients. These patients have more atrophy in their brains making vessels more likely to rupture.

37
Q

extradural haemorrhage

A

Extradural haemorrhage is usually caused by rupture of the middle meningeal artery in the temporo-parietal region. It can be associated with a fracture of the temporal bone. It occurs between the skull and dura mater. On a CT scan they have a bi-convex shape and are limited by the cranial sutures (they can’t cross over the sutures).

The typical history is a young patient with a traumatic head injury that has an ongoing headache. They have a period of improved neurological symptoms and consciousness followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents.

38
Q

intracerebral haemorrhage

A

Intracerebral haemorrhage involves bleeding into the brain tissue. It presents similarly to an ischaemic stroke.

These can be anywhere in the brain tissue:

  • Lobar intracerebral haemorrhage
  • Deep intracerebral haemorrhage
  • Intraventricular haemorrhage
  • Basal ganglia haemorrhage
  • Cerebellar haemorrhage

They can occur spontaneously or as the result of bleeding into an ischaemic infarct or tumour or rupture of an aneurysm.

39
Q

Subarachnoid Haemorrhage

A

Subarachnoid haemorrhage involves bleeding in to the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.

subarachnoid haemorrhage has a very high mortality and morbidity. It is very important not to miss the diagnosis and you need to have a low suspicion to trigger full investigations. It needs to be discussed with the neurosurgical unit with a view to surgical intervention.

80% caused by berry aneursym rupture

40
Q

mx of intracranial bleeding

A
  • Immediate CT head to establish the diagnosis
  • Check FBC and clotting
  • Admit to a specialist stroke unit
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
41
Q

presentation of subarachnoid haemorrhage

A

The typical history is a sudden onset occipital headache that occurs during strenuous activity such as weight lifting or sex. This occurs so suddenly and severely that it is known as a “thunderclap headache”.

It is described like being hit really hard on the back of the head. Other features are:

  • Neck stiffness
  • Photophobia
  • Vision changes
  • Neurological symptoms such as speech changes, weakness, seizures and loss of consciousness

They are particularly associated with cocaine and sickle cell anaemia.

42
Q

RFs for subarachnoid haemorrhage

A
  • Hypertension
  • Smoking
  • Excessive alcohol consumption
  • Cocaine use
    • Family history

Subarachnoid haemorrhage is more common in:

  • Black patients
  • Female patients
  • Age 45-70

It is particularly associated with:

  • Cocaine use
  • Sickle cell anaemia
  • Connective tissue disorders (such as Marfan syndrome or Ehlers-Danlos)
  • Neurofibromatosis
    • Autosomal dominant polycystic kidney disease
43
Q

Ix for subarachnoid haemorrhage

A

Immediate CT head is required. Blood will cause hyperattenuation in the subarachnoid space.

if CT head negative - then LP is done >12 hrs AFTER headache onset to check for:

CSF Red cell count will be raised. If the cell count is decreasing in number over the samples, this could be due to a traumatic lumbar puncture.

CSF Xanthochromia (the yellow colour of CSF caused by bilirubin)

Angiography (CT or MRI) can be used once a subarachnoid haemorrhage is confirmed to locate the source of the bleeding.

44
Q

Mx of subarachnoid haemorrhage

A

Patients should be managed by a specialist neurosurgical unit. Patients with reduced consciousness may require intubation and ventilation.

refer to neurosurgery immediately

nimodipine

surgery: endovascular coiling vs surgical clipping

Surgical intervention may be used to treat aneurysms. The aim is to repair the vessel and prevent re-bleeding. This can done by coiling, which involves inserting a catheter into the arterial system (taking an “endovascular approach”), placing platinum coils into the aneurysm and sealing it off from the artery. An alternative is clipping, which involves cranial surgery and putting a clip on the aneurysm to seal it.

Nimodipine is a calcium channel blocker that is used to prevent vasospasm. Vasospasm is a common complication that can result in brain ischaemia following a subarachnoid haemorrhage.

Lumbar puncture or insertion of a shunt may be required to treat hydrocephalus.

Antiepileptic medications can be used to treat seizures.

Supportive care as part of a multi-disciplinary team is important with good nursing, nutrition, physiotherapy and occupational therapy involved during the initial stages and recovery.

45
Q

signs and symptoms of raised ICP

A

headache - chronic, progrssive, worse on walking, lying, bending forward, coughing.

vomiting, papilloedema, seizures, localiszing signs, odd behaviour.

LP is CI until after imaging

46
Q

headache with eye pain+/- reduced vision diff

A

acute glaucoma - typically elderly, long sighted. unilateral pain arnd one eye radiating to forehead with reduced vision, visual haloes and a red congested eye. seek expert help at once. if delay in tx of > 1hr is likely, give eye drops (timolol maleate +/- pilocarpine) and PO acetazolamide

GCA - subacute headache, raised ESR. exclude in all >50 yr. prompt diagnosis and steroids to avoid blindness

acute episode of cluster headahce

47
Q

migraine and females

A

COCP CI in women with migraine + aura

low dose cocp can be used in those without aura

prganancy - migraine often improves; if not get help - greater risk of pre-eclampsia. paracetamol 1st line. don’s use aspirin if breast feeding. antiemetic choic - cyclizine or promethazine

48
Q

meningitis? meningococcal septicaemia?

A

inflammation of the meninges usually due to a bacterial or a viral infection.

The most common causes of bacterial meningitis in children and adults is Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus). less commonly H. infleunzae

In neonates the most common cause is Group B Streptococcus (GBS). GBS is usually contracted during birth from the GBS bacteria that can often live harmlessly in the mothers vagina.

Neisseria meningitidis is a gram negative diploccous bacteria. Meningococcal septicaemia is the cause of the classic “non-blanching rash” that everybody worries about as it indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages.

Meningococcal meningitis is when the bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord.

49
Q

presentation of meningitis

A

fever, neck stiffness, vomiting, headache, photophobia, abnormal skin colour, altered consciousness, shock: prolonged CRT, hypotension, DIC, and, seizures. Where there is meningococcal septicaemia - non-blanching rash. Other causes of bacterial meningitis do not usually cause the non-blanching rash.

50
Q

presentation of meningitis in neonates and babies

A

Neonates and babies can present with very non-specific signs and symptoms such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle. For this reason NICE recommend lumbar puncture as part of the investigations for all children:

  • Under 1 months presenting with fever
  • 1 – 3 months with fever and are unwell
    • Under 1 years with unexplained fever and other features of serious illness
51
Q

special tests you can perform to look for meningeal irritation:

A

Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.

Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.

52
Q

Management of Bacteria Meningitis

A

it is a medical emergency. ix and tx proceed in parallel

ABCDE

pts seen in community with suspected meningitis AND a non blanching rash should receive an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important. This shouldn’t delay transfer. Where there is a true penicillin allergy transfer should be the priority rather than other antibiotics.

in hospital -

ABCDE , fluid resus and IVI if req. check and correct blood glucose.

ideally blood culture and LP for CSF culture and sensitivities before starting abx however abx shd not be delayed esp if septicaemic

Send blood tests for meningococcal PCR if meningococcal disease is suspected. (faster than BC)

low threshold for tx. Always follow the local guidelines however typical antibiotics are:

  • < 3 months and >60 yrs or immunocompcefotaxime plus amoxicillin (the amoxicillin is to cover listeria contracted during pregnancy from the mother)
  • > 3 monthsceftriaxone

Vancomycin should be added to these if there is a risk of penicillin resistant pneumococcal infection such as from recent foreign travel or prolonged antibiotic exposure.

GET ICU help if signs of raised ICP (reduced GCS, papilloedema, seizures, focal neurology) or septicaemic (shock, evolving rash)

Dexamethasone if features of meningism are also used in bacterial meningitis to reduce the frequency and severity of hearing loss and neurological damage.

Bacteria meningitis and meningococcal infection are notifiable diseases so public health need to be informed of all cases.

basically -

ABCDE

airway and breathing support if required

get IV access

take blood cultures

fluid resus if req

start IV abx +/- call ITU

+/- dex

LP when stable and raised ICP ruled out

53
Q

post exposure prophylaxis for meningococcal infection

A

The risk of highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness.

Post exposure prophylaxis is guided by public health. The usual antibiotic choice for this is a single dose of PO ciprofloxacin. It should be given as soon as possible and ideally within 24 hours of the initial diagnosis.

54
Q

viral meningitis causes, mx

A

herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV). A sample of the CSF from the lumbar puncture should be sent for viral PCR testing.

Viral meningitis tends to be milder than bacterial and often only requires supportive treatment. Aciclovir can be used to treat suspected or confirmed HSV meningitis.

55
Q

LP puncture site?

A

The spinal cord ends at the L1-L2 vertebral level so the needle is usually inserted into the L3-L4 intervertebral space. Samples are sent for bacterial culture, viral PCR, cell count, protein and glucose.

A blood glucose sample should be sent at the same time so that it can be compared to the CSF sample. The samples need to be sent immediately.

56
Q

bacterial vs viral LP results

A

It makes sense that bacteria swimming in the CSF will release proteins and use up the glucose. Viruses don’t use glucose but may release a small amount of protein. The immune system releases neutrophils in response to bacteria and lymphocytes in response to viruses.

57
Q

complications of meningitis

A
  • Hearing loss is a key complication
  • Seizures and epilepsy
  • Cognitive impairment and learning disability
  • Memory loss
  • Focal neurological deficits such as limb weakness or spasticity
58
Q

some additional causes of meningitis in immunocompromised pts

A

CMV, cryptococcus and TB

59
Q

when to suspect encephalitis

A

odd behaviour, reduced consciousness, focal neurology or seizure preceeded by an infectious prodrome (raised temp, rash, lymphadenopathy, cold sores, conjunctivitis, meningeal signs). often wise to treat before exact cause is known as it is usually viral.

if no infectious prodrome consider encephalopathy: hypoglycaemia, hepatic encephalopathy, DKA, drugs, hypoxic brain injury, uraemia, SLE, wernicke’s (give vit B1 if in doubt)

60
Q

causes of encephalitis

A

viral: HSV 1&2, arboviruses, CMV, EBZ, VZV, HIV, measels, mumps, rabies

non-viral: bacterial meningitis, TB, malaria, lyme disease, listeria, legionella, cryptococcus, leptospirosis, autoimmune

61
Q

Ix for encephalitis

A

blood cultures, serum for viral PCR, throat swab and MSU, toxoplasma IgM titre, malaria film

contrast enhanced CT: focal bilateral temporal lobe involvement is suggestive of HSV encephalitis. do before LP.

LP - CSF protein, cells, glucose and viral PCR

EEG- urgent EEG can confirm encephalitis but doesnt indicate cause

62
Q

mx of encephalitis

A

untreated encephalitis mortality - 70%

start IV aciclovir within 30 mins of pt arriving as empirical treatment for HSV. specific therapies for CMV and toxoplasmosis

supportive therapy in ICU/HDU environment if necessary

symptomatic tx: eg phenytoin for seizures

63
Q

cerebral abscess: when to suspect?

ix

mx

A

in any pt with raised ICP, esp if fever or rasied WCC

there may be hx of ear, ssinus, dental, periodontal infection, skull fracture, endocarditis, congenital heart disease, bronchiectasis

signs: seizures, fevers, localising signs, signs of raised ICP, coma, signs of sepsis/infection

ix - CT/MRI (ring enhancing lesion), raised WCC, raised ESR, biopsy

Mx - ABCDE, urgent neurosurgical referral, treat raised ICP.

is patient immunocompromised??

discuss with ID/microbiology

64
Q

raised ICP causes, presentation, ix and mx

A

pg830

65
Q

IIIrd nerver palsy at presentation of a SAH gives what hint?

A

that there may be an anaeurysm in the posterior communicating artery or an intracerebral haematoma pressing on the IIIrd nerve

66
Q

complications of SAH

A

rebleeding

cerebral ischaemia due to vasospasm

hydrocephalus due to blockage of arachnoid granulations

hyponatraemia (seek expert help. shd NOT be managed with fluid restriction)

67
Q

diff types of brain tumours

A

They vary from benign tumours (e.g. meningiomas) to highly malignant (e.g. glioblastomas).

1.Secondary Metastases

The common cancers that metastasise to the brain are:

  • Lung
  • Breast
  • Renal cell carcinoma
  • Melanoma

2.Gliomas

Gliomas are tumours of the glial cells in the brain or spinal cord. There are three types to remember (listed from most to least malignant):

  • Astrocytoma (glioblastoma multiforme is the most common)
  • Oligodendroglioma
  • Ependymoma

Gliomas are graded from 1-4. Grade 1 are most benign (possibly curable with surgery). Grade 4 are the most malignant (glioblastomas).

3.Meningiomas

Meningiomas are tumours growing from the cells of the meninges in the brain and spinal cord. They are usually benign, however they take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms.

4.Pituitary Tumours

Pituitary tumours tend to be benign. If they grow large enough they can press on the optic chiasm causing a specific visual field defect called a bitemporal hemianopia. They have the potential to cause hormone deficiencies (hypopituitarism) or to release excessive hormones leading to:

  • Acromegaly
  • Hyperprolactinaemia
  • Cushing’s disease
  • Thyrotoxicosis

5.Acoustic Neuroma (AKA Vestibular Schwannoma)

Acoustic neuromas are tumours of the Schwann cells surrounding the auditory nerve that innervates the inner ear. They occur around the “cerebellopontine angle” and are sometimes referred to as cerebellopontine angle tumours. They are slow-growing but eventually grow large enough to produce symptoms and become dangerous.

Acoustic neuromas are usually unilateral. Bilateral acoustic neuromas are associated with neurofibromatosis type 2.

Classic symptoms of an acoustic neuroma are:

  • Hearing loss
  • Tinnitus
  • Balance problems

They can also be associated with a facial nerve palsy.

6. primary CNS lymphoma (non infectious manifestation of HIV)

7. cerebellar tumours

68
Q

Presentation of brain tumours

A

asymptomatic (esp when they are small)

As they develop they present with focal neurological symptoms depending on the location of the lesion. (eg personality change in frontal lobe tumours)

symptoms and signs of raised intracranial pressure

69
Q

raised ICP signs and symptoms

A

Papilloedema is a key finding on fundoscopy

Altered mental state
Visual field defects
Seizures (particularly focal)
Unilateral ptosis
Third and sixth nerve palsies

headache - Constant Nocturnal Worse on waking Worse on coughing, straining or bending forward Vomiting

70
Q

fundoscopic changes in papilloedema

A
  • Blurring of the optic disc margin
  • Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
  • Loss of venous pulsation
  • Engorged retinal veins
  • Haemorrhages around optic disc
    • Paton’s lines which are creases in the retina around the optic disc
71
Q

Managing Brain Tumours

A

Management options include:

  • Palliative care
  • Chemotherapy
  • Radiotherapy
  • Surgery

Surgery is dependent on the grade, location and behaviour of the brain tumour.

Treatment of Pituitary Tumours

  • Trans-sphenoidal surgery
  • Radiotherapy
  • Bromocriptine to block prolactin-secreting tumours
    • Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours
72
Q

idiopathic intracranial hypertension

A

present - headache raised ICP and NO intracranial mass found

also narrowed visual firelds, blurred vision +/- diplopia, VIth nerve palsy, enlarged blind spot. consciousness and cognition preserved

most commonly obese females

associated with endocrine abnormalities, CKD, drugs (steroids, oral contraceptives, etc), SLE

Ix - CT Head to rule out SOL

Mx - wt loss, acetazolamide or topiramate, loop diuretics, prednisolone. consider optic nerve sheath fenestration or lumbar-peritoneal shunt if drugs fail and visual loss worsens

often self-limiting but permanent significant visual loss in 10%

73
Q

neuropathic pain definition

A

pain arising as a direct consequence of a lesion or disease affecting the somatosensory system

74
Q

causes of neuropathic pain

A

Peripheral

  • Postherpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk
  • Nerve damage, including postoperative.
  • Diabetic neuralgia typically affects the feet
  • Trigeminal neuralgia
  • Pain because of cancer tumour infiltration.
  • Alcohol neuropathy

Central

  • Multiple sclerosis
  • Post-stroke pain.
  • chemo induced pain

not sure where this fits - Complex Regional Pain Syndrome (CRPS)

75
Q

typical features of neuropathic pain

A
  • Burning
  • Tingling
  • Pins and needles
  • Electric shocks
    • Loss of sensation to touch of the affected area
      • The pain may be provoked by normally innocuous stimuli (allodynia). Neuropathic pain is also commonly associated with hyperalgesia (increased pain intensity evoked by normally painful stimuli), paraesthesia and dysaesthesia.
76
Q

what is used to assess the characteristics of the pain and examination of the affected area in neuropathic pain

A

DN4 Questionnaire

They are then scored out of 10 for their pain. A score of 4 or more indicates neuropathic pain.

77
Q

mx of neuropathic pain

A

treatment of underlying cause

Non-pharmacological measures:

  • Physiotherapy to maintain strength
  • Psychological input to help with understanding and coping
  • NICE recommends the use of spinal cord stimulation in patients who have had chronic pain for six months (measuring at least 50 mm on a 0-100 mm visual analogue scale) despite conventional medical management

medications used -

  • Offer a choice of -
  • Amitriptyline is a tricyclic antidepressant
  • Gabapentin is an anticonvulsant
  • Pregabalin is an anticonvulsant
  • Duloxetine is an SNRI antidepressant

Other options:

  • Tramadol ONLY as a rescue for short term control of flares
  • Capsaicin cream (chilli pepper cream) for localised areas of pain who wish to avoid, or who cannot tolerate, oral treatments.

Trigeminal neuralgia is a type of neuropathic pain however NICE recommend carbamazepine as first-line for trigeminal neuralgia and if that does not work to refer to a specialist.

78
Q

complex regional pain syndrome

A

This is a condition where areas are affected by abnormal nerve functioning causing neuropathic pain and abnormal sensations. It is usually isolated to one limb. Often it is triggered by an injury to the area.

The area can become very painful and hypersensitive even to simple inputs such as wearing clothing. It can also intermittently swell, change colour, change temperature, flush with blood and have abnormal sweating and hair growth.

Treatment is often guided by a pain specialist and is similar to other neuropathic pain.

79
Q

radiculopathy vs radicular pain

A

Radiculopathy is a neurological state in which conduction is limited or blocked along a spinal nerve or its roots.

Radicular pain is usually caused by compression of the nerve root due to disc herniation or degenerative spondylotic changes, but radicular symptoms can also occur without evident compression (for example, due to inflammation of the nerve).

they commonly occur together.

Cervical radiculopathy is the term used to describe the pain in one or both of the upper extremities which corresponds to the dermatome of the involved cervical nerve root.

80
Q

causes of cervical radiculopathy

A

degenerative changes, including osteoarthritis, cervical disc herniation (22 per cent of cases), spondylosisand trauma

81
Q

S&S of cervical radiculopathy

A

Pain in the neck, shoulder and/or arm that approximates to that of a dermatome.

Sensory symptoms

Motor symptoms

Postural asymmetry. if the asymmetry is long-standing, muscle wasting may be present.

Neck movements — these may be restricted or painful

Dural irritation — assess with the Spurling test.

Neurological problems — for example, upper limb weakness, paraesthesia, dermatomal sensory or motor deficit, or diminished tendon reflexes at the appropriate level. Nerve root symptoms should normally arise from a single nerve root — involvement of more than one nerve root suggests a more widespread neurological disorder.

82
Q

most common nerve root affected in cervical radiculopathy?

A

The most common nerve root affected is C7, followed by C6.

83
Q

from C5 to T1 - nerve root affected, muscle weakness, reflex changes and sensory changes table

A
84
Q

red flags in someone presenting with neck pain

A

Fever.
Generalised neck stiffness.
Lymphadenopathy.
Nausea or vomiting.
Pain that is increasing, is unremitting, or disturbs sleep.
Severe neck tenderness.
Skin erythema, wounds or exudate.
Unexplained weight loss.
Neurological problems like altered mental status, UMN signs

A history of inflammatory arthritis, cancer, tuberculosis, immunosuppression, drug abuse, AIDS, or other infections.

New symptoms before the age of 20 years or after the age of 55 years.

85
Q

ddx for neck pain

A

Thoracic outlet syndrome

Acute disc prolapse

Acute torticollis

Acute trauma

Adverse drug reactions (for example, antipsychotic drugs, metoclopramide, amphetamines, cocaine).

Arthritis of cervical spine.

86
Q

mx of cervical radiculopathy

A

If cervical radiculopathy has been present for less than 4–6 weeks and there are no objective neurological signs, provide conservative management:

Provide reassurance and information

Encourage activity (including home exercise) and a return to a normal lifestyle (including work) as soon as possible.

Offer oral analgesics

advise firm pillow may help

consider amitriptyline, duloxetine, pregabalin or gabapentin; physiotherapy; muscle relaxants

If cervical radiculopathy has been present for 4–6 weeks or more, or there are objective neurological signs:

magnetic resonance imaging (MRI) to confirm diagnosis

consider invasive procedures, such as interlaminar cervical epidural injections, transforaminal injections, or spinal surgery.

Indications for surgery include signs and symptoms of cervical radiculopathy with unremitting radicular pain despite 6 to 12 weeks of conservative treatments, or progressive motor weakness, and MRI that shows nerve root compression.