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Neurology Flashcards

1
Q

What is the difference between Conus Medullaris Syndrome and Cauda Equina?

A

Conus Medullaris- Upper Motor Neurone signs- Hyperreflexia and Hypertonia

Cauda Equina- Lower Motor Neurone signs- Hyporeflexia and Hypotonia

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2
Q

What are the 4 causes of Cauda Equina?

A

Lumbar Disc Herniation

Trauma (Fall)

Spinal Tumour

Lumbar Spine Stenosis (narrowing of the spinal canal)

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3
Q

What are the 5 signs of Cauda Equina?

A

Lower Back pain and Sciatica (Back and Leg Pain)

Saddle Anaesthesia- numbness in the Peri-anal Region, Groin and Inner Thighs

Urinary Retention and Incontinence (Palpable Bladder due to Urinary Retention)

Leg Weakness and Difficulty Walking

Erectile Dysfunction

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4
Q

What 2 investigations should be done if Cauda Equina is suspected?

A

Urgent MRI of the Spine

CT Myelography if an MRI is not possible

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5
Q

What is the management of Cauda Equina?

A

Emergency Decompressive Laminectomy Surgery

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6
Q

What are Cluster Headaches and what is their pahtophysiology?

A

They are Unilateral, Periorbital Headaches with Autonomic Dysfunction that presents with (4) Conjunctival Infection, Lacrimation, Rhinorrhoea and Nasal Congestion

They are a form of Trigeminal Autonomic Cephalgia that occur due to the Hypersensitivity of the Trigeminal Autonomic Reflex Arc- they consist of Vascular Dilation and Trigeminal Nerve Stimulation

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7
Q

What are the 3 main forms of Trigeminal Autonomic Cephalgia?

A

Cluster Headaches

Paroxysmal Hemicranial

Short-lived Unilateral Neuralgiform Headaches with Conjunctival Injection and Tearing (SUNCT)

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8
Q

What are the 8 signs of Cluster Headaches?

A

Clusters of Headaches that occur due to certain precipitants (Alcohol, Volatile smells, Warm temperatures, Sleep)

Unilateral, Periorbital or Temporal headaches that last between 15 mins to 3 hours

Ipsilateral Autonomic Symptoms (6)

  • Lacrimation
  • Conjunctival Infection
  • Nasal Congestion
  • Rhinorrhoea
  • Ptosis
  • Miosis
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9
Q

What investigation should be conducted if a Cluster Headache is suspected?

A

ESR- to rule out Giant Cell Arteritis

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10
Q

What is the management of Cluster Headaches? (3)

What 4 things should be avoided? (4)

A

Triptans for Symptomatic Relief
High flow Oxygen
Verapamil for Prophylaxis

Avoid

  • Paracetamol
  • NSAIDs
  • Opioids
  • Oral Triptans
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11
Q

What is the most common cause of Encephalitis?

A

Herpes Simplex Virus 1

causing Frontal and Temporal Lobe Encephalitis

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12
Q

What is the main risk factor for Encephalitis?

A

Being Immunocompromised (HIV, being Very Old or Very Young, Medication)

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13
Q

What are the 6 signs of Encephalitis?

A

Reduced GCS

Fever

Headache (Excruciating)

Confusion

Focal Neurological Deficit (3)

  • Aphasia
  • Hemiparesis
  • Cerebellar signs

Behavioural Changes (3)

  • Memory disturbances
  • Psychotic behaviour
  • Withdrawal or changes in personality
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14
Q

What 3 investigations should be ordered if Encephalitis is suspected?

A

MRI- would show inflammation of Frontal and Temporal Lobes in Herpes Simplex Virus 1

Cerebrospinal Fluid- Lymphocytosis with Raised Protein in Viral Aetiology

EEG- Periodic Lateralised Discharges at 2Hz

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15
Q

What is the 3 step management plan for Encephalitis?

A

Aciclovir

Ganciclovir- If it is a Herpes Virus that is Not HSV1

Ganciclovir and Foscarnet- If it is Cytomegalovirus

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16
Q

What is the pathophysiology of Guillain-Barre Syndrome?

A

It is an autoimmune demyelinating condition of the Peripheral Nervous System- triggered by an Infection

  • This is due to a pathogenic antigen being very similar to Myelin Gangliosides in the Peripheral Nervous System
  • So the Myelin Sheath is attacked by the Immune System
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17
Q

What are the 2 types of Guillain-Barre Syndrome and what are some facts about them?

A

Acute-Inflammatory Demyelinating Polyneuropathy (ADIP) is the most common

Miller-Fischer Syndrome (3)

  • Ataxia, Areflexia and Opthalmoplegia
  • In this form, the Eyes are affected first- not the Legs like Normal
  • It is a Descending Paralysis
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18
Q

What are the two main risk factors for Guillain-Barre Syndrome?

A

Malignancies- Lymphoma may increase risk of Guillain-Barre Syndrome

Respiratory or Gastrointestinal Infections-

Bacterial (2)

  • Campylobacter Jejuni
  • Mycoplasma Pneumoniae

Viral (4)

  • Zika virus
  • Influenza
  • Epstein-Barr Virus
  • Cytomegalovirus
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19
Q

What are the 6 signs of Guillain-Barre Syndrome

A

Symmetrical Muscle weakness affecting the Legs first and then the Arms (Ascending Weakness)

Tingling in hands and feet which is followed by muscle weakness

Unsteady when Walking- Ataxia with Hyporeflexia or Areflexia in Affected Limb

Back and Leg Pain

Shortness of Breath- due to weakness of Respiratory Muscles

Facial Weakness and Speech Problems- Cranial Nerve Involvement and Bulbar Dysfunction (Diplopia or Facial Droop)

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20
Q

What 6 investigations should be conducted if Guillain-Barre Syndrome is suspected?

A

Progressive Weakness and Areflexia (hyporeflexia) typically means Guillain-Barre Syndrome

Check B12 and Folate as their deficiencies are associated with Neurological Features

TFTs- to exclude Hypothyroidism as a cause of Weakness

LFTS- elevation of Hepatic Enzymes is associated with a more Severe Disease

Anti-Ganglioside Antibodies- as AntiGQ1b is associated with Miller-Fisher Syndrome

Lumbar Puncture- shows Raised Protein with Normal WBC Count (However a Normal Protein Level does NOT Exclude Guillain-Barre Syndrome)

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21
Q

What is the 5 step management for Guillain-Barre Syndrome?

A

IV Immunoglobulins

Plasma Exchange

Thromboprophylaxis to Prevent Venous Thromboembolisms

Physiotherapy

Intensive Care Support

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22
Q

What are the 3 complications of Guillain-Barre Syndrome?

A

Type 2 Respiratory Failure

Pulmonary Complications (such as infections due to Intubation or Pulmonary Emboli due to immobility and a pro-inflammatory state

Autonomic Dysfunction of Bowel (ileus) and Bladder (retention)

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23
Q

What are the 8 red flags for a Headache?

A

Recent Head Trauma (within past 3 months)- check for Subdural Haematoma

Headache worse when standing- check for a CSF leak

Headache worse when lying down- check for a raised ICP (such as due to a Space-Occupying Lesion)

Household contact has similar symptoms (check for CO poisoning)

Headache with a Fever or a Change in Consciousness (check for Meningitis or Encephalitis)

Headache with Visual Disturbance (check for Acute Closed Glaucoma)

Headache with Vomiting (check for a Space-occupying Lesion, Abscess or CO Poisoning)

Headache during Pregnancy (check for Pre-Eclampsia)

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24
Q

What 4 conditions can a Lumbar Puncture help diagnose?

A

Multiple Sclerosis
Guillain-Barre Syndrome
Sub-Arachnoid Haemorrhage
Meningitis

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25
Q

What are the 6 contraindications for a Lumbar Puncture?

A 
Raised ICP (Papilloedema)
Change in Consciousness
Shock
Bradycardia and Hypertension (part of Cushing's Triad)
Issues with Pupils
After a Convulsion
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26
Q

What are the 2 most common causes of Bacterial Meningitis?

A

Streptococcus Pneumoniae and Neisseria Meningitidis

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27
Q

What is the most common cause of Viral Meningitis?

A

Coxsackievirus

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28
Q

What are the 9 signs of Meningitis?

A

Meningism (Headache, Stiffness, Photophobia)

Fever

Nausea and Vomiting

Seizures

Petechial or Purpuric Non-blanching Rash- due to Neisseria Meningitidis

Kernig’s Sign- unable to extend knee when the hip is flexed

Brudzinski Sign- hips and knees flex when the neck is also flexed

Reduced GCS

Bulging Anterior Fontanelle (Top of baby’s head where there is a gap in the skulls usually is bulging)

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29
Q

Which 6 investigations should be ordered if Meningitis is suspected?

A

FBC- check for Leukocytosis

Coagulation Screen before Lumbar Puncture

Check Blood Glucose in ALL Patients too compare with CSF Glucose

Perform a whole blood PCR for Neisseria Meningitidis

Perform a CSF PCR for Herpes Simplex Virus and Varicella Zoster Virus

Perform a CSF Gram Stain- Streptococcus Pneumoniae is a Gram Positive Cocci and Neisseria Meningitidis is a Gram Negative Diplococci

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30
Q

What is the 5 step management for Meningitis?

A

IV or IM Benzylpenicillin

Do NOT offer antibiotics in Primary Care as this will delay the transfer to the hospital

Steroids- Dexamethasone is ideally given With or Before the Antibiotics

Antibiotics (2)

  • Cefotaxime (add Amoxicillin if they are <3 months or >50 years old)
  • Give Chloramphenicol if they are allergic to Penicillin

For Viral Meningitis- give Aciclovir

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31
Q

What are the 4 complications of Meningitis?

A

Hydrocephalus

Cerebral Oedema

Sensorineural Hearing Loss

Waterhouse-Friderischsen Syndrome- Adrenal Gland Failure due to a Haemorrhage caused by Neisseria Meningitidis

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32
Q

What are 6 things to note in the CSF interpretation of Meningitis?

A

The Pressure is only normal in Viral Meningitis, but it may be elevated or normal in Bacterial and Fungal Meningitis and Tuberculosis

The Fluid Appearance is only Clear in Viral Meningitis, it is Cloudy in Bacterial and Fungal Meningitis and Tuberculosis

If the White Cell Count in the CSF is over 1,000, this is Bacterial Meningitis, although the White Cell Count may be normal in Bacterial Meningitis as well

The main cells visible in the CSF in Bacterial Meningitis and early stages of other Meningitis are Neutrophils, and Lymphocytes in the later stages of Viral and Fungal Meningitis and Tuberculosis

The Protein in the CSF would only be less than 1g/L in Viral Meningitis

The Glucose in the CSF would only be greater than 60% in Viral Meningitis

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33
Q

What is the most likely cause of Meningitis in Neonates and the most likely cause of Meningitis in Very Old People and Very Young People?

A

Group B Streptococcal Bacteria are the most common cause of Meningitis in Neonates

Listeria Monocytogenes is the most common cause of Meningitis in Very Old and Very Young Patients

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34
Q

What should be offered to people who have been in close contact with patients diagnosed with Meningitis ? (3)

A

Ciprofloxacin (first line)

Rifampicin (second line)

Meningococcal Vaccination

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35
Q

What is the pathophysiology of a Migraine?

A

It is thought to occur due to the Hyperexcitability of the Trigeminal Nerve which dilates the Meningeal Blood Vessels and causes Sensitisation of Surrounding Nerve Fibres which causes the Pain

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36
Q

What are the triggers of a Migraine? (CHOCOLATE +3)

A 
Chocolate
Oral Contraception
Alcohol
Anxiety
Travel
Exercise

Bright Lights
Lack of Food and Water
Menstruation

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37
Q

What are the 4 signs of a Migraine?

A

Unilateral Pulsing Headache (commonly Bilateral in Children)

Photophobia and Phonophobia

Typical Aura (up to 1 hour) (3)-

  • Visual Symptoms
  • Paresthesia
  • Speech Disturbances

Atypical Aura (more than 1 hour) (4)

  • Poor Balance
  • Diplopia
  • Motor Weakness
  • One eye only affected
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38
Q

What 2 investigation should be ordered if a Migraine is suspected?

A

CT or MRI to rule out other causes such as a Subarachnoid Haemorrhage

ESR to rule out Giant Cell Arteritis

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39
Q

What is the management plan for Acute (4) and Chronic (7) Migraine?

A

Acute Migraine-

  • Ibuprofen or Aspirin or Paracetamol
  • Oral Sumatriptan (Alone or in combination with Paracetamol and NSAIDs)
  • Antiemetic (Metoclopramide or Prochlorperazine)
  • Avoid Opiates!!!

Chronic Migraine-
- Headache Diary
Prophylaxis-
- Propanolol (First Line)
- Topiramate (unless the patient is Pregnant)
- Amitriptyline
- Frovatriptan or Zolmitriptan if the patient is having Predictable Menstrual Migraines
- Otherwise Consider Mindfulness and Acupuncture
- Riboflavin may be good but avoid in Pregnancy

40
Q

What are the 4 types of Motor Neurone Disease and state some facts about each of them?

A

Amylotrophic Lateral Sclerosis (ALS)-

  • Mutations in SOD1
  • Upper Motor Neurone Signs- Predominantly affects the Corticospinal Tracts
  • Lower Motor Neurone Signs- also affects Anterior Horn Cells

Progressive Muscle Atrophy-

  • Lower Motor Neurone Signs- Predominantly affects the Anterior Horn Cells
  • Best Prognosis

Primary Lateral Sclerosis-
- Upper Motor Neurone Signs- Predominantly affects the Corticospinal Tracts

Progressive Bulbar Palsy-

  • Affects the Suprabulbar Nuclei and Cranial Nerves- causes Speech and Swallowing Issues
  • Worst Prognosis
41
Q

What are the 5 signs of Motor Neurone Disease?

A

Falls

Progressive Weakness

Speech and Swallow Issues- Mainly in Progressive Bulbar Palsy
- Dysarthria and Dysphagia are mainly seen in Progressive Bulbar Palsy

Fasciculations (especially in the Tongue)- are also seen in Motor Neurone Disease

Muscle Wasting- look out for Atrophies

42
Q

What 3 investigations should be ordered if Motor Neurone Disease is suspected?

A

Electromyography (evidence of Fibrillation Potentials)

Nerve Conduction Studies show Reduction in Amplitude

Pulmonary Function should be assessed as Motor Neurone Disease Patients are at risk of Respiratory Failure

43
Q

What is the 5 step management of Motor Neurone Disease?

A

Riluzone

Respiratory Support in Patients with a Reduced FVC (like BiPAP)

Supportive treatments-

  • Antispasmodics (Baclofen)
  • Feeding support- from a PEG tube
  • Speech and Language Therapy
  • Physiotherapy
44
Q

What are the 2 complications of Motor Neurone Disease?

A

Respiratory Failure

Aspiration Pneumonia and Bronchopneumonia

45
Q

What is the pathophysiology of Multiple Sclerosis?

A

It is an autoimmune Demyelinating Disease of the Central Nervous System

46
Q

What are the 2 patterns of Multiple Sclerosis?

A

Relapsing-Remitting- which is the most common

Primary/ Secondary Progressive- which has no remission associated with it

47
Q

What are the 5 risk factors of Multiple Sclerosis?

A

Epstein-Barr Virus

HLA-DR2

Vitamin D Deficiency

Living in Northern Latitudes

Autoimmunity

48
Q

What are the 8 signs of Multiple Sclerosis?

A

Optic Neuritis (3)-

  • Blurred Vision and Red Desaturation
  • Pale Optic Disc
  • Unilateral or Bilateral Internuclear Opthalmoplegia (one eye doesn’t move as much to the left or right as the other)

Numbness and Tingling

Sensory Loss due to Demyelination of the Spinothalmic or the Dorsal Columns

Upper Motor Neuron Signs with Spastic Paraparesis

Bowel and Bladder Dysfunction

Uhtoff’s Phenomenon- The Symptoms get worse with an Increased Temperature- like in a Hot Bath

Lhermitte’s Phenomenon- Electric Shock Sensation on Neck Flexion

Cerebellar Signs- Ataxia and Tremor

49
Q

What 3 investigations should be ordered if Multiple Sclerosis is suspected?

A

MRI of the brain and spine-

  • Demyelinating plaques would be seen (Dawson’s Fingers are found Perpendicular to the Lateral Ventricles)
  • High Signal T2 Lesions

Oligoclonal Bands on Lumbar Puncture, also an increased IgG

EEG= Visual-Evoked Potentials- Delayed Velocity but a Normal Amplitude

50
Q

What is the management of Multiple Sclerosis? Relapsing (2) and Maintenance (4)

A

Relapsing-

  • Steroids (Oral or IV Methylprednisolone) is first line
  • Plasma Exchange if this does not work

Maintenance- DMARDs

  • Beta Interferon (reduces the Relapse Rate but Not the Progression)
  • Monoclonal Antibodies (Natalizumab and Alemtuzumab) reduce the Relapse Rate and the Progression
  • Glatiramer Acetate- an immunomodulator which acts as a Decoy
  • Fingolimod- which keeps the Lymphocytes in the Lymph Nodes
51
Q

How should the complications of Multiple Sclerosis be managed? (5)

A

Fatigue- Investigate other causes (like Anaemia) and consider giving them Amantidine

Spasticity- Physiotherapy- Gabapentin and Baclofen are first line

Mental Health Issues- Amitryptilline

Bladder Dysfunction- Intermittent self-catheterisation if there is a Significant Residual Volume

Anticholinergics should be given if the Bladder Residual Volume is Insignificant

52
Q

What is the pathophysiology of Myasthenia Gravis?

A

It is a Chronic Autoimmune Disorder of the Post-synaptic Membrane at the Neuromuscular Junction of Skeletal Muscles

This occurs due to antibodies against Nicotinic Acetylcholine Receptors

Some patients have antibodies against Muscle-Specific Kinase (MuSK) which is a post-synaptic protein

The number of available binding sites for Acetylcholine at the muscle is reduced and this causes weakness

53
Q

What are the 2 risk factors of Myasthenia Gravis?

A

Thymoma/ Thymic Hyperplasia

Autoimmunity

54
Q

What are the 9 signs of Myasthenia Gravis?

A

Fatigability

Diplopia- as the Extraocular Muscles are the first to be affected

A Muscle Weakness that is worse at the end of the day

Proximal Muscle Weakness with Fatigability

Ptosis which is exacerbated on an upward gaze (Bilateral or Unilateral)

Dysphagia

Myasthenia Snarl (Snarling expression when attempting to smile)

Head Drop- this is a rare sign which occurs due to a weakness of the Cervical Extensor Muscles

Complex Opthalmoplegia- which can not be attributed to one Cranial Nerve

55
Q

What 4 investigations should be ordered if Myasthenia Gravis is suspected?

A

Antibodies (Against the Acetylcholine Receptors and Muscle-Specific Kinase)

Electrophysiological Studies- repetitive nerve stimulation shows a Decremental Muscle Response

CT to exclude a Thymoma

TFTs- as there is a prevalence of Autoimmune Thyroiditis

56
Q

What is the 6 step management of Myasthenia Gravis?

A

Pyridostigime is first line (it is an Acetylcholinesterase Inhibitor)

Prednisolone is second line (if Pyridostigime doesn’t change the symptoms)

Azathioprine is third line (if Prednisolone does not work)

Use Methotrexate or Rituximab if the symptoms are uncontrolled by the first three medications

Perform a thymectomy if a thymoma is present

If the patient has Myasthenia Crisis (Myasthenia Gravis with weakened Respiratory Muscles)-

  • IV Immunoglobulins or Plasmapheresis
  • Intubation (if severe)
  • Corticosteroids
57
Q

What are the 2 complications of Myasthenia Gravis?

A

Myasthenic Crisis

Aspiration Pneumonia- as Dysphagia increases the risk of Aspiration

58
Q

What 9 drugs should be avoided in Myasthenia Gravis?

A 
Tetracyclines
Ciprofloxacin
Gentamicin
Quinolones
Azithromycin
Beta Blockers
Procainimide
Lithium
Phenytoin
59
Q

What are 4 signs of Parkinsonism?

A

Bradykinesia
Tremor
Rigidity
Postural Instability

60
Q

What 4 diseases are associated with Parkinsonism?

A

Parkinson’s Disease- Unilateral Symptoms which then become Bilateral as the Disease Progresses

Parkinson plus Syndrome (3)

  • Multiple System Atrophy (Shy Drager Syndrome)
  • Progressive Supranuclear Palsy (Vertical Gaze Palsy)
  • Corticobasal Degeneration (Alien Limb Phenomenon)

Lewy Body Dementia

  • Cognitive Impairment
  • Visual Hallucinations

Wilson’s Disease
- Parkinsonism and Liver Failure with Kayser-Fleischer Rings

61
Q

What are the 4 drugs and 3 other things that can causes Parkinsonism?

A

Antipsychotics
Metoclopromide (an antiemetic)
Domperidone (an antiemetic)
Lithium

Encephalitis
Illegal Drugs
Dementia Pugilistica

62
Q

What is the pathophysiology of Parkinson’s Disease?

A

It is the loss of Dopaminergic Neurones in the Substantia Nigra Pars Compacta of the Basal Ganglia

It is associated with a Dysfunction in the genes associated with Alpha Synuclein and Ubiquitin Protease-

  • This leads to a loss of transmission between the Basal Ganglia, Thalamus and Motor Cortex
  • This results in an impaired Voluntary Movement
63
Q

What is the protein found in Parkinson’s Disease?

A

Lewy Bodies- Eosinophilic Inclusion Bodies consisting of misfolded Alpha Synuclein in the Substantia Nigra Pars Compacta

64
Q

What are the 7 signs of Parkinson’s Disease?

A

Bradykinesia

Tremor (Pill Rolling Tremor)

Rigidity (Cog Wheel Rigidity)

Anosmia (an early feature)

Sleep Disturbance

Constipation

Psychiatric Symptoms (Depression, Anxiety, Dementia which develops after the Motor Symptoms)

65
Q

What 2 investigations should be ordered if Parkinson’s Disease is suspected?

A

MRI Brain- to exclude other possibilities

SPECT (DaT scan) to show Reduced Dopamine Uptake in Basal Ganglia

66
Q

What is the 8 step management of Parkinson’s Disease?

A

If the Quality of Life is affected-
- Levodopa and Decarboxylase Inhibitor (Co-Beneldopa)

If Quality of Life is Not Affected (give One of These)

  • Levodopa and Decarboxylase Inhibitor (Co-Beneldopa)
  • Dopamine Agonist (Pramipexole or Ropinirole), Avoid Bromocroptine as it leads to Cardiac Fibrosis and Pulmonary Fibrosis
  • Monoamine Oxidase B Inhibitor (Selegiline or Rasagiline)

If the Above don’t work-

  • Entacapone- reduces Breakdown of Levodopa Peripherally meaning that More of it reaches the brain
  • Amantidine- increases Dopamine Release and reduces Uptake
  • Subcutaneous Apomorphine- Dopamine Agonist
  • Deep Brain Stimulation
67
Q

What is Status Epilepticus?

A

It is a Single Continuous Seizure lasting more than 5 minutes or 2 Consecutive Seizures

68
Q

What are the 7 risk factors for Status Epilepticus?

A

Epilepsy

Poor compliance with Anti-epileptic Medication

Alcoholism

Recreational Drug Use (Cocaine)

Previous Neuronal Injury (5)

  • Head Trauma
  • Stroke
  • Haemorrhage
  • Brain Tumours
  • CNS Infection

Electrolyte Imbalance- particularly Hyponatraemia and Hypocalcaemia

Medications (4) reduce their threshold-

  • Buproprion
  • Tramadol
  • Theophylline
  • Certain Antibiotics
69
Q

What are the 5 signs of Status Epilepticus?

A

Tonic-clonic Seizure- Muscles stiffen and Jerking of Limbs occur

Tongue biting

Urinary Incontinence

Loss of Consciousness

Post Ictal- Confusions and Altered State of Consciousness After and Epileptic Seizure

70
Q

What 5 investigations should be ordered if Status Epilepticus is suspected?

A

ECG- look for Cardiac Arrhythmias as these can Precipitate Seizures

Arterial or Venous Blood Gases- Metabolic Acidosis with Raised Lactate

Inflammatory Markers to identify a possible infection

Investigate Anti-epileptic Drug levels

Perform Toxicology Screen

71
Q

What is the 6 step management for Status Epilepticus?

A

If the patient has Alcohol Excess= Give them Pabrinex or Glucose

If any two Benzodiazepines have been given- move on to the Established Status Treatment

Pre-Hospital=

  • Rectal Diazepam or Buccal Midazolam
  • If the seizure continues then proceed…

Early Status (<10 minutes)=

  • IV Lorazepam is First Line in Hospital
  • If this still continues, then proceed…
Established Status (10-60 minutes)=
- Phenytoin and/ or Phenobarbital

Refractory Status (60-90 minutes)=

  • General Anaesthesia with (3)
  • Propofol
  • Midazolam
  • Thiopental
72
Q

What are the 2 complications of Status Epilepticus?

A

Aspiration Pneumonia/ Respiratory Failure

Hyperkalaemia and Hypoglycaemia

73
Q

What are the 3 types of Haemorrhagic Stroke?

A

Intracerebral- bleeding within the brain Parenchyma

Subarachnoid- bleeding into the Subarachnoid space

Intraventricular- bleeding within the Ventricles- Prematurity is a strong risk factor for this

74
Q

What are the Cardiac (3), Vascular (2) and Haematological (3) causes of Ischaemic Stroke?

A

Cardiac

  • Atherosclerotic Disease (4)- Smoking, Hypertension, Diabetes, Hypercholesterolaemia
  • Atrial Fibrillation
  • Embolism due to Septal Abnormality- such as Patent Foramen Ovale

Vascular

  • Aortic Dissection
  • Vertebral Dissection

Haematological

  • Hypercoagulability- Antiphospholipid Syndrome
  • Sickle Cell Anaemia
  • Polycythaemia
75
Q

What are the 4 causes of Haemorrhagic Stroke?

A

Trauma

Arteriovenous Malformation

Intracerebral Strokes in Particular (Hypertension and Cerebral Amyloid)

Subarachnoid Strokes in Particular (Berry Aneurysm)

76
Q

What are the signs of Anterior Cerebral Artery Strokes?

A

Contralateral Hemiparesis and Sensory Loss in the Lower Limbs more than the Upper Limbs

77
Q

What are the signs of Middle Cerebral Artery Strokes?

A

Contralateral Hemiparesis and Sensory Loss in the Lower Limbs more than the Upper Limbs

Homonymous Hemianopia-

  • Aphasia if the Dominant Hemisphere is affected, as the Wernicke’s Area is Affected
  • Hemineglect Syndrome- if Non-Dominant Hemisphere is affected
78
Q

What are the signs of Posterior Cerebral Artery Strokes?

A

Contralateral Homonymous Hemianopia with Macular Sparing

Contralateral loss of Pain and Temperature due to Spinothalamic Damage

79
Q

What are the signs of Vertebrobasilar Artery Strokes?

A

Cerebellar Signs

Reduced Consciousness

Quadriplegia or Hemiplegia

80
Q

What are the signs of Weber’s Syndrome Strokes (due to a Midbrain Infarct)?

A

Oculomotor Palsy

Contralateral Hemiplegia

81
Q

What are the signs of Lateral Medullary Syndrome Strokes (due to Posterior Inferior Cerebral Artery Occlusion)?

A

Ipsilateral Facial loss of Pain and Temperature

Ipsilateral Horner’s Syndrome (Ptosis, Miosis, Anhidrosis, Enophthalmos)

Ipsilateral Cerebellar Signs

Contralateral loss of Pain and Temperature

82
Q

What 4 investigations should be ordered if a Stroke is suspected?

A

Non-Contrast CT Head to work out whether it is a Haemorrhagic or an Ischaemic Stroke (Ischaemic would not show up)

ECG for Atrial Fibrillation

Blood tests- Check for Risk Factors and Rule out the 2 Stroke Mimics (Hypoglycaemia and Hyponatraemia)

CT Angiogram for Artery Occlusion

83
Q

What is the 6 step management for an Ischaemic Stroke?

A

Give them Aspirin ASAP
- but if they are treated with Thrombolysis then start Aspirin 24 hours after the Haemorrhage is excluded on the Non-Contrast CT Head

Start Thrombolysis if they are within 4.5 hours of Symptom onset and Haemorrhagic Strokes are excluded on imaging

Perform Thrombectomy if they are >5 on the NIH Scale and <3 on the Rankin Scale

Do NOT Start Anticoagulation if Atrial Fibrillation is the cause and give them Aspirin instead

Also Maintain their Blood Glucose levels

Secondary Prevention (3)-

  • Clopidogrel is First Line
  • Otherwise give them Aspirin with Dipyridamole
  • All Patients should be started on a high-dose statin such as Atorvastatin
84
Q

What is the management of a Haemorrhagic Stroke?

A

It depends on the subtype

For Subarachnoid Haemorrhage- Endovascular or Surgical Clipping

Admit Haemorrhagic Stroke Patients to Neurocritical Care and monitor for Raised Intracranial Pressure
(Consider Intubation with Hyperventilation, Head Elevation 30 degrees and IV Hypertonic Saline)

Decompression via Surgery may be needed

85
Q

What 3 arteries are associated with the Anterior Circulation of the head and which 5 arteries are associated with the Posterior Circulation of the head?

A

Anterior Circulation-

  • Anterior Choroidal Artery
  • Anterior Cerebral Artery (ACA)
  • Middle Cerebral Artery (MCA)

Posterior Circulation-

  • Posterior Cerebral Artery (PCA)
  • Basilar Artery
  • Superior Cerebral Artery
  • Anterior Inferior Cerebellar Artery
  • Posterior Inferior Cerebellar Artery
86
Q

What are Berry Aneurysms? (2)

A

Ruptures of Saccular Berry Aneurysms are the most common cause of spontaneous Subarachnoid Haemorrhages

They occur at points of Arterial Bifurcation within the Circle of Willis- such as the junction between the Anterior Communicating Artery and Anterior Cerebral Artery- which is the Most Common Location

87
Q

What are Watershed Zones within the Head and give 2 examples of them?

A

These are areas that are Furthest away from Arterial Supply and are therefore vulnerable to Reduced Perfusion

1) Cortical Border Zone Infarction- border of the ACA/ MCA and the MCA/PCA
2) Internal Border Zone Infarction- borders of the penetrating MCA branches or borders of the deep branches of the MCA and ACA- deep white matter infarction

88
Q

Which artery supplies the Wernicke’s and Broca’s Area?

A

The Middle Cerebral Artery

89
Q

Why does Macular Sparing Occur in Strokes?

A

The Occipital Pole is responsible for supplying the Macula and this region has a rich Anastomoses of vessels- this region is supplied by the MCA

90
Q

What is Locked-In Syndrome?

A

The patient is fully aware but can not move or communicate verbally due to almost complete paralysis

This may be caused by a Stroke affecting the Basilar Artery so that no blood is delivered to the Pons

91
Q

What is the most common cause of a Subarachnoid Haemorrhage?

A

Trauma

92
Q

What are the 4 Atraumatic Causes of a Subarachnoid Haemorrhage?

A

Berry Aneurysm- Most Common Cause of Spontaneous Subarachnoid Haemorrhage

  • This arises at a point of Arterial Bifurcation within the Circle of Willis
  • The junction between the Anterior Cerebral Artery and Anterior Communicating Artery is the most common location
  • This is associated with Polycystic Kidney Disease, Coarctation of Aorta and Ehler’s-Danlos Syndrome

Arteriovenous Malformation

Mycotic Aneurysm- due to Bacterial Infection- like secondary to Emboli from Infective Endocarditis

Pituitary Apoplexy- Bleeding into the Pituitary Gland, associated with a Tumour

93
Q

What are the 2 risk factors of a Subarachnoid Haemorrhage?

A

Polycystic Kidney Disease

Alcohol

94
Q

What are the 7 signs of a Subarachnoid Haemorrhage?

A

Headache (Occipital, Thunderclap Headache and Sudden Onset)

Meningism- Photophobia and Neck Stiffness

Nausea and Vomiting

Confusion, Coma and Seizures

Reduced GCS

3rd Nerve Palsy- from Posterior Cerebral Artery Aneurysm pressing on the 3rd nerve- Dilated Pupil

6th Nerve Palsy- Increases ICP

95
Q

What 4 investigations should be ordered if a Subarachnoid Haemorrhage is suspected?

A

Urgent non-contrast CT of head- Blood in Basal Cisterns

ECG should be done on ALL patients (Arrhythmias and ST Elevation)

If the CT is negative but you are still suspicious of a Subarachnoid Haemorrhage, then perform a Lumbar Puncture-
- Xanthochromia with Normal or Raised Opening Pressure (Xanthochromia is the yellow pigmentation of the CSF due to the degradation of Haemoglobin to Bilirubin)

CT Angiogram or DSA (Digital Subtraction Angiography)- to find the Source

96
Q

What is the 5 step management for Subarachnoid Haemorrhage?

A

Nimlodipine should be offered immediately

Endovascular Clipping of the Aneurysm is the first line investigation

Surgical Clipping via Craniotomy is second line

If the ICP is raised- perform Intubation with Hyperventilation, Head Elevation to 30 degrees and IV Mannitol

Prescribe Antitussives and Stool Softeners to prevent patient straining and reduces risk of rebleeding

97
Q

What are the 3 main complications with Subarachnoid Haemorrhage?

A

Vasospasm (Treat with induced Hypervolaemia, Hypertension, Haemodilution)

Hydrocephalus- manage via External Ventricular Drain

Hyponatraemia due to SIADH

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