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Phase 3A DJF > Neurology > Flashcards

Neurology Flashcards

Learn me!!

1
Q

Define titubation

A

A tremor causing a nodding movement of the head (or body) often in a yes-yes-no-no way

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2
Q

Define dysphonia

A

Difficulty with speech due to physical disorder of mouth, tongue, palate or vocal cords

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3
Q

Define dysarthria

A

Poor articulation of speech that is otherwise linguistically normal

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4
Q

Define dysphasia

A

Difficulty with language (but not physical production of sounds)

Can be expressive or receptive

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5
Q

How do you test for dysphasia?

A

Give a one stage command and if successful continue with more complex commands. Write down words if necessary.
Expressively dysphasic patients will be able to follow commands but not answer questions making any sense.

Also ask patients to name objects. Receptively dysphasic patients often get the idea and can name the object, but expressively dysphasic patients cannot.

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6
Q

How do you test for dysphnia?

A 
Say:
Pa pa pa  (Facial muscles)
Ta ta ta    (tongue)
Ka ka ka  (Soft palate)
Baby hippopotamus
British constitution
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7
Q

What treatment should a patient receive before, during and following a stem cell transplant?

A

Before: Adjuvant chemotherapy

During: Diuretic

After: 
Antifungal (fluconazole) 6 months
Antiviral (Acyclovir) 12 months
Antibiotic (Trimethoprim) 6 months
Antiemetic (Donperidone) PRN
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8
Q

What is the age limit for stem cell transplant

A

46

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9
Q

From where are stem cell transplant cells taken

A

The patient - Autologous transplant (replaced after being treated)

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10
Q

What are the potential complications of stem cell transplants?

A

Hyperthyroid

Loss of memory B cells

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11
Q

What two phenomena combine to cause cogwheel rigidity? What condition is this finding suggestive of?

A

Tremor and rigidity

Parkinsonism

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12
Q

What does the short synactin test test for?

A

Hypoadrenalism

Synactin is given at 9am with bloods taken at 9 and 9:30am to assess response

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13
Q

What is the typical posture of a patient with pyramidal weakness?

A

Upper limb(s) flexed, lower limb(s)s extended

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14
Q

What condition presents with mixed upper and lower motor neuron signs?

A

Motor neuron disease

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15
Q

What three ways can motor neuron disease present?

A

Limb
Respiratory
Bulbar (speech and swallowing)

NB: Any onset can spread to involve the other two as the disease progresses

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16
Q

What is the treatment for MND?

A

Riluzole - extends life expectancy by ~3 months

Symptomatic support

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17
Q

What does the acronym IDEAL stand for?

A

Stroke inpatient necessities:

Imaging
DVT prophylaxis
ECG
Anticoagulation/antiplatelet
Lab tests
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18
Q

Which is closer to the midline of the brain, putamen or globus pallidus?

A

Globus pallidus

Putamen is Peripheral!

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19
Q

Can you co-prescribe Clopidogrel and Omeprazole?

A

No, they interact.

Prescribe Clopidogrel and LANSOPRAZOLE

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20
Q

When should Creatinine Kinase be tested?

A 
When a patient is suspected to have spent a long period of time immobile (eg stroke and found on floor)
High CK (in thousands) shows Rhabdomyelysis and likely AKI
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21
Q

How do you test for colour blindness?

A

Ishihara plates

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22
Q

What types of colourblindness are there?

A

Red-Green.
Less sensitive to red = Protanopia
Less sensitive to green = Deuteranopia

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23
Q

Is colour blindness more common in one gender?

A

Yes, males

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24
Q

How do you treat discitis?

A

IV Flucloxacillin and IV Rifampicin

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25
Q

What do you see on imaging of a SAH?

A

Starfish on base of skull

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26
Q

What do you see on imaging of extradural haemorrhage?

A

Biconvex blood accumulation between brain and skull, possible midline shift

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27
Q

What do you see on imaging of subdural haemorrhage?

A

Crescent shaped blood around edge of cortical grey matter

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28
Q

What can be caused by co-prescribing antiepileptic and antpsychotic drugs?

A

Terminal Ileus

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29
Q

What is assessed when a lumbar puncture is taken?

A

WCC - Infection marker
Protein - Inflammation marker
Xanthochromia - RBC breakdown product (bleeds)
Pressure - RIP

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30
Q

Define a semantic error in aphasia

A

Substituting a different word which describes a different object (eg saying clock instead of watch)

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31
Q

Define a phonic error in aphasia

A

Substituting a different word which sounds similar (eg saying witch instead of watch)

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32
Q

In what timeframe would a vascular event present?

A

Instantly

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33
Q

In what timeframe would an inflammatory event present?

A

3-6 Weeks

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34
Q

In what timeframe would an infective event present?

A

3-6 Weeks

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35
Q

In what timeframe would a degenerative event present?

A

Months to Years

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36
Q

Describe Hoover’s sign

A

A test for functional symptoms - if unilateral leg weakness is described, feel the weak leg while asking patient (lying on couch) to flex strong leg at the hip.
If positive the weak leg will use normal power to balance body while strong leg is being flexed.

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37
Q

By what other name are functional symptoms called?

What is the cause of functional symptoms?

A

Somatisation syndrome

Caused by past intolerable, unacceptable stress that patient has no control over. Memories of this stress are too difficult for the body to handle and so it avoids them by distracting itself with functional symptoms. This is most commonly childhood trauma, especially sexual abuse.

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38
Q

If a stroke patient is having speech problems, how might you figure out the location of the stroke?

A

If patient has aphasia it is likely to be cortical, test for expressive and receptive dysphasia.

If patient has dysarthria it is likely to be a brainstem or cerebellar stroke.

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39
Q

T/F, a patient with a brainstem stroke is likely to complain of double vision

A

True.

Cortical strokes rarely cause double vision

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40
Q

What can cause hemiparesis?

A 
Stroke
Hemiplegic migraine
Todd's paresis (follows epileptic attack)
Hypoglycaemia
Functional symptoms
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41
Q

How is a lumbar puncture performed?

A

Procedure and SEs described and consent gained.
Patient is laid on side. Line drawn between ASISs and intervertebral gap identified. Site cleaned and lidocaine injected. Skin needle inserted followed by non-cutting LP needle that passes through tissues and into dura. Needle core removed and CFS flows out slowly. Opening pressure is measured (should be between 12-20cm. 5 bottles then filled with 10 drops CSF and closing pressure measured (between 4th and 5th pots). Needles removed and dressing applied.
Procedure documented.

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42
Q

What are the potential side effects of a LP?

A

Low pressure headache
Meningeal tear (if low pressure headache continues over 2 days)
Infection
Bleeding

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43
Q

For what is Botox injection a treatment?

A

Muscular dystonia (of face or cervical spine)
Injections every 8-12 weeks to relax muscles.
Overtreatment in bulbar region can cause swallowing difficulties

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44
Q

What is a serious psychiatric side effect of antiepileptic drugs?

A

Suicidal ideation

Most frequent with Levetriacetam

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45
Q

What can cause vertigo?

A

Labyrinthitis
BPPV - Benign Positional Paroxysmal Vertigo
Drugs (antiepileptics, antidepressants)
Vestibular migraine

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46
Q

What is BPPV, how is it caused and how is it treated?

A

Benign Positional Paroxysmal Vertigo
Intermittent vertigo initiated by specific movement(s). Frequently involves vomiting and swaying.
Caused by Otoliths, which are crystals in the labyrinth of semicircular canals that get stuck in certain positions.
Treated with Epley manouvre (tilting head to one side, lay down, tilt head to other side, sit up.

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47
Q

Define penumbra

A

The area around a stroke focus that experiences reduced bloodflow and without treatment will also die, but is salvageable with quick treatment.

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48
Q

Describe a spastic gait

A

Circumduction, no bending of the knee, often bilateral

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49
Q

Describe a hemiplegic gait

A

Unilateral circumduction, extended leg with foot drop but flexed ipsilateral arm

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50
Q

Describe a fastodian gait

A

Aka Shuffling gait

difficulty initiating, difficulty turning, small steps, reduced arm swing, stooped posture

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51
Q

Describe a high steppage gait

A

Walking with foot drop, so high steppage is required to avoid scraping toes along floor

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52
Q

Describe a waddling gait

A

Pelvic drop with upper body compensation creating the waddling appearance

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53
Q

Describe an ataxic gait

A

Wide base, unstable

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54
Q

Describe a gait involving chorea

A

Chorea = involuntary movements, therefore the gait is difficult and random, varying speed. Balance is unaffected however

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55
Q

Describe an antalgic gait

A

Limping due to pain

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56
Q

What conditions can cause a spastic gait?

A

MS
Cord compression
Genetic causes

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57
Q

What conditions can cause a hemiplegic gait?

A

Stroke

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58
Q

What conditions can cause a fastodian gait?

A

Parkinsomism

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59
Q

What conditions can cause a high steppage gait?

A

Peripheral neuropathy

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60
Q

What conditions can cause a waddling gait?

A

Proximal myopathy

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61
Q

What conditions can cause an ataxic gait?

A

Cerebellar lesions

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62
Q

Describe status epilepticus

A

NOT self-limiting siezures that occur before recovery is made or (rarely) continuously. Greater than 30 mins without stopping is definite, greater than 5 minutes without stopping is highly suggestive.
Can be tonic-clonic, Focal, Absence or Myoclonic but tonic-clonic status is the only emergency.

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63
Q

What can cause status epilepticus?

A

Changes or withdrawal of antiepilepsy meducations, learning disabilities or structural brain lesions.

Can also occur in non-elipeltics caused by alcohol, encephalitis, hypoglycaemia, ampheamines, hyponatruaemia, hypocalcaemia, stroke

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64
Q

What features are useful for differentiating epileptic from non-epileptic attacks?

A 
In epileptic siezures:
Eyes closed (Open in non-epileptic)
Mouth open (closed in non-epileptic)
Incontinence common (rare in non-epileptic)
Tongue biting on side
Rhythmic tonic-clonic movements (steady tremor that rarely stops is more non-epileptic)
Hyperprolactinaemia
High CK 
High lactate
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65
Q

What investigations should you do in status epilepticus?

A 
Blood glucose 
U+E
Temperature
ESR
CRP
Tox screen
CT head
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66
Q

How would you treat status epilepticus?

A

Benzodiazepines (IV Lorazepam or sublingual/rectal diazepal), two doses 10 mins apart

2nd line try Levotriacetam or Phenyotoin

Refer to ICU and use general anaesthesia if necessary

IV Thiamine (eg Pabrinex)

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67
Q

What causes Guillian-Barre syndrome?

A

Previous GI or URT infection, most commonly campylobacter (diarrhoea)
Can also be EBV, H influenzae or Mycoplasma pneumoniae

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68
Q

What are the symptoms of GBS?

A

Progressive, ascending weakness 1-3 weeks post infection, with or without paraesthesia
Can involve facial or bulbar muscles
Gradual loss of reflexes
Back pain

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69
Q

What is the prognosis for GBS?

A

Symptoms worst 2 weeks post onset
Self limiting but slow recovery.
30% remain disabled.

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70
Q

What is the diagnosis? and 3 differentials

A patient presents with progressive, ascending weakness and paraesthesia. This is associated with back pain.
On examination there are absent ankle reflexes.
They admit to having had a cold 3 weeks ago.

A

Guillian Barre Syndrome

Differentials:
Botulism
Cord compression
Myasthenia gravis

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71
Q

What investigations would you do in GBS?

A

Serum IgA (deficiency leads to anaphylaxis with IVIg treatment)
LP (high protein, normal WCC)
NCS (slow conduction due to demyelination)

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72
Q

How is GBS managed?

A

IVIg or Plasmapheresis
Gabapentin (neuropathic pain)
Physiotherapy
ITU (Resp ventillation, SALT assessment, Cardiac assessment, all if necessary)

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73
Q

How does Miller Fisher syndrome present?

A

Progressive ophthalmoplegia and ataxia. Pure sensory variant of GBS

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74
Q

What is the incidence of SAH?

A

1 in 10,000 (UK)

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75
Q

What causes SAH?

A

Berry aneurysm rupture
Traumatic or infectious aneurysm
Clotting disorder/anticoagulation
Dural Arterio-Venous Malformation

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76
Q

What are the symptoms of SAH?

A

Thunderclap headache with instant onset mostly associated with strenuous activity.
Neck stiffness (pain on flexion of neck or spine)
Photophobia
Coma or lowered GCS
Positive Kernig’s sign

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77
Q

What is the diagnosis?

80 year old male presents with an intense headache that started in an instant while he was getting out of bed. His neck is stiff and he is covering his eyes.
His wife reports he is slowly becoming more confused.

A

Subarachnoid heamorrhage

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78
Q

What investigations should be done for SAH?

A

CT head on day of admission
LP (RBCs or Xanthochromia, high opening pressure)
CT angiogram
Bloods (U+E, FBC, clotting)

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79
Q

How is SAH managed?

A 
Bed rest with head elevated at 45 degrees
ABCDE+resus if low GCS
Fluids (over 3L/day to avoid vasospasm)
Nill By Mouth
Analgesia
Antiemetics
Aneurysm clipping or coiling
Nimodipine (CCB for hypertension)
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80
Q

What is the prognosis for SAH?

A

Rule of thirds:
33% recover completely
33% recover partially
33% fatal

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81
Q

What is the prevalence of meningitis?

A

2-3 per 100,000

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82
Q

What are the possible routes of meningitis infection?

A

ears
nasopharynx
cranial injury
blood stream

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83
Q

What infectious agents can cause meningitis?

Which causes the non-blanching rash?

A 
Bacteria:
Strep. pneumoniae
Staph. aureus
Neisseria meningitidis *causes the non-blanching rash
TB
Viruses:
HIV
Herpes simplex
Epstein-Barr virus
Mumps

Fungi:
Candida albicans
Cryptococcus neoformans

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84
Q

What are the symptoms of meningitis?

A

Headache
Fever
Photophobia
Neck stiffness

CN 3,4,6,8 palsies
focal neurological deficits
siezures
raised ICP
non-blanching rash
weight loss (if TB caused)
Vomiting
Kernig's sign positive
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85
Q

What is the diagnosis?

20 year old female presents with her student flatmate suffering with a headache, fever and neck stiffness. She is wearing sunglasses indoors.

A

Meningitis

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86
Q

What investigations do you do for meningitis?

A

Blood cultures
CXR
CT head
LP (if possible)

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87
Q

What is the management of meningitis?

A

Emperical antibiotics:
With rash - Benzylpenicillin or cefotaxime
No rash - Cefotaxime, Vancomycin & Ampicillin

Then follow microbiology guidance from MC&S

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88
Q

What can cause raised intracranial pressure?

A

Mass lesions
Venus sinus thrombosis
Hydrocephalus

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89
Q

What can result because of raised intracranial haemorrhage? What are the types of this?

A

HERNIATION
Cingulate - cingulate gyrus under falx
Central - Diencephalon through tentorial incisura (pituitary stalk may be sheared or PCA compressed)
Uncal - Uncus or hippocampus over edge of tentorium (confusion, CNIII palsy, coma, contralateral weakness)
Upward cerebellar - vermis above tentorium (Compression of SCA, veins and aqueduct causing hydrocephalus. Anaxia, unequal fixed pupils, low GCS. Caused by posterior fossa mass)
Tonsillar - Cerebellar tonsils through foramen magnum (ataxia, CN VI palsy, low GCS, rapidly fatal. Can be post-LP)

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90
Q

How is cranial herniation managed?

A

IV Mannitol 20% bolus (removes fluid from brain)
Sedation
Treat the cause (neurosurgery referral)

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91
Q

What can cause encephalitis?

A

Mostly viral:
Herpes simplex
Varicella Zoster
Autoimmune

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92
Q

What are the symptoms of encephalitis?

A 
Fever
Acute confusion
New siezures
Personality change
Lowered GCS
focal neurological defecits
(Hyponatraemia if AI)
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93
Q

What is the diagnosis:

A 65 year old female presents with a fever, acute confusion and lowered GCS. Her husband reports her to be acting up a bit.
On examination she has weakness of her left side with ipsilateral sensation disturbance.

A

Viral encephalitis

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94
Q

What is the diagnosis:

A 65 year old male presents with a new seizure that has left him confused, drowsy and not quite himself. He has lost sensation in his right arm.
On investigation, you find his blood Na to be low.

A

AI encephalitis

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95
Q

What investigations should be done for encephalitis?

A

CT/MRI head
LP (lymphocytosis, high protein, PCR of CSF for herpes simplex virus)

Autoantibodies in CSF or serum (anti-VGKC)

96
Q

What is the management for viral encephalitis?

A

IV acyclovir for 21 days

IV phenytoin if siezures

97
Q

What is the management for AI encephalitis?

A

IVIg

High dose steroids

98
Q

What are the symptoms of CN III palsy?

A

Fixed dilated pupils
Partial or complete ptosis
Weakness of MR, SR, IR and IO (down and out eyes)

Mostly unilateral

99
Q

What are the symptoms of Horner’s syndrome?

A

Pinpoint pupils (still reactive to light and accomodation reflex)
Partial or upside-down ptosis
Anhydrosis
Enophthalmos

1% Hydroxyamphetamine dilates pupil temporarily

100
Q

What is the prevelance of Myasthenia gravis?
Gender equality?
Peak incidence?

A

5-12 per 100,000
Twice as common in FEMALES
Peak incidence 30s

101
Q

What conditions are associated with Myasthenia gravis?

A 
Thyroiditis
Graves' disease
Rheumatoid arthritis
SLE
Pernicious anaemia
Addison's disease
Vitiligo
102
Q

Describe the pathophysiology of Myasthenia gravis

A

Reduced number of nicotinic ACh receptors at NMJ
Conformal change increasing gap of NMJ
Therefore, decreased amplitude of endplate potentials with failure to trigger a muscle action potential.
Fatigue occurs as increasing numbers of fibres fail to fire.

103
Q

What are the symptoms of Myasthenia gravis?

A

Painless muscle weakness that is FATIGUEABLE
Mostly starts with occular muscles then spreads to bulbar (dysphasia, dysphagia, dysarthria, jaw or neck weakness) and limbs
Exacerbated by hypothyroidism, infection or drugs

Normal sensations and reflexes

104
Q

What is the diagnosis:

54 year old male presents with blurred vision when staring at objects or later in the day. Recently his legs have been tiring quicker than usual for him too.
On examination he has normal sensations and reflexes

A

Myasthenia gravis

105
Q

What investigations do you do for Myasthenia gravis?

A

Serum AChR antibody (PATHOGENIC)
Repetitive nerve stimulation
Single fibre EMG (shows delayed or failed transmissions)
MRI/CT thorax (thymoma - 75% MG patients have thymomas)
Tensilon test - Give Edrophonium, weakness improves within 5 mins but can also cause bronchospasm and syncope)
Vertical and horizontal FVC

106
Q

What is the management for MG?

A 
Cholinesterase inhibiters (Pyridostigmine) - can cause abdo pain and diarrhoea
Thymectomy (or steroids of can't do operation)
Azathioprine (T-cell specific immunosuppressant)
107
Q

What can cause a Myasthenic crisis?

A

Medication non-compliance
Infection
Drugs (Antibiotics, Beta-blockers, CCBs, Antipsychotics, Statins, Li)

108
Q

How does a Myasthenic crisis present?

What else can present in a similar way?

A

Expressionless face (slack facial muscles)
Head drop (weak neck muscles)
Slack Jaw
Absent gag reflex
Respiratory distress (inability to cough) and rapid shallow breathing

*Cholinergic crisis presents in similar way (MG overtreatment)
But you also get:
Salivation
Lacrimation
Urinary incontinence
Diarrhoea
GI upset
Emesis
109
Q

What is the diagnosis:

You enter a ward to find a patient with an expressionless face, dropping head and mouth wide open. Their breathing is rapid and shallow.

A

Myasthenic crisis

110
Q

How is Myasthenic crisis investigated?

A

CXR (for aspiration)
CT/MRI chest (Thymoma)
Tensilon test
Ice pack on eyes can resolve ptosis and facial droop

111
Q

How is Myasthenic crisis managed?

A 
ABCDE
Treat cause (most frequently infection)
Oral Pyridostigmine if no cause found
112
Q

Define hydrocephalus

A

Excessive accumulation of CSF caused by disturbed flow, formation or absorption.
Normal CSF production is 500ml per 24 hours.
Total CSF volume in adults is 125 ml (so recycled 3 times a day)

113
Q

What can cause acute hydrocephalus?

A 
Posterior fossa tumour
Stroke
Colloid of 3rd ventricle
SAH
Traume
Acute meningitis
114
Q

What can cause chronic hydrocephalus?

A

SAH
Chronic meningitis
Slow growing posterior fossa tumours

115
Q

What are the symptoms of acute hydrocephalus?

A 
Increased ICP
Headache
Vomiting
Diplopia (CN VI palsy)
Reduced GCS
LOC or sudden death
116
Q

What are the symptoms of chronic hydrocephalus?

A

Gait distrubance and apraxia
Dementia or memory disturbance
Urinary incontinence
Raised ICP headache symptoms

117
Q

What investigations should be done in hydrocephalus?

A

CT/MRI head (ventricular enlargement with temporal horns becoming visible. Balloning of frontal horns and 3rd ventricle. Thinned or bowed corpus callosum. Large or small 4th ventricle depending on type)

118
Q

What is the management of hydrocephalus?

A

Ventricular-Peritoneal shunt
Endoscopic 3rd ventriculostomy
Serial LP or external lumbar drain

119
Q

What can go wrong with cerebral shunts?

A

CSF protein >4g/L will clog shunt

120
Q

Define normal pressure hydrocephalus

A

Chronic communicating hydrocephalus with normal CSH pressure. Classically idiopathic but can follow trauma or infection

121
Q

What are the symptoms of normal pressure hydrocephalus?

A

(Hakim-Adams triad:)

Gait disturbance (apraxia - instability despite normal power and sensations, cycling movement preserved)
Cognitive impairment (gradual slowing of verbal and motor responses leading to apathetic or depressed appearance)
Urinary incontinence
122
Q

What investigations should normal pressure hydrocephalus require?

A 
CT head (enlarged ventricles etc but normal sulci/gyri)
MRI head (no loss of hippocampal volume, which would normally allow temporal horn enlargement. Bowed corpus callosum)
123
Q

How is normal pressure hydrocephalus managed?

A

Ventricular-Peritoneal shunt

124
Q

What is the diagnosis:

A 38 year old male presents with a headache, vomiting, double vision and drowsiness. His symptoms get worse when he coughs, strains or leans forwards.

A

Acute hydrocephalus

125
Q

What is the diagnosis:

A 64 year old male presents with a long history of difficulty walking, memory disturbances, urinary incontinence and headache, which is worse when he coughs or bends forwards.

A

Chronic hydrocephalus

126
Q

What is the incidence of MND?
Age of onset?
Gender equality?

A

2 per 100,000
age 50-75
Males more likely below 70, equal thereafter

127
Q

Describe the pathogenesis of MND

A

Motor neurons of the spinal cord (upper and lower), cranial nerves and coretex affected by protein aggregation in the axons. This causes oxidative damage leading to progressive destruction of the neurons.

128
Q

What are the symptoms of MND?

In what three ways can these symptoms present?

A 
Asymmetrical onset of weakness in upper or lower limb
Dysarthria
Dysphagia
Muscle wasting
Fasciculations (esp. tongue)
Brisk reflexes
Extensor plantar response

Sensory examination intact

3 ways: BULBAR, LIMB or OCCULAR

129
Q

What is the prognosis for Progressive Bulbar Palsy MND?

A

2-3 years

130
Q

What is the prognosis for limb onset MND?

A

3-4 years

131
Q

What is the prognosis for Progressive muscular atrophy MND?

A

5-10 years

132
Q

What is the prognosis for Primary lateral sclerosis MND?

A

15 years

133
Q

What causes MND?

A

Genetics (AD condition or AR spinal atrophy)
Infections (HIV, Poliomyelitis)
Prion disease
Toxins (Lead, Mercury)

134
Q

What investigations should MND require?

A 
FBC, ESR, Ca, Glucose, TFT
Autoantibodies screen
CXR
MRI spine
EMG
NCT
135
Q

What is the management of MND?

A 
Riluzole - gives 3 months extra on life expectancy
MND specialist nurse
Physio and OT
SALT and dietician
Palliative care
136
Q

What is the diagnosis:

A 49 year old female presents with weakness of the left arm up to the elbow and weakness of the right hand to the wrist.
On examination her muscles are starting to waste in the weak areas, fasciculations are noted on the left side and her reflexes are brisk. Sensations intact.

A

MND (Limb onset)

137
Q

What is the diagnosis:

A 54 year old man presents with difficulty swallowing and a new speech impediment. He struggles to say words correctly but does not tire towards the end of sentences. He can swallow fluids but struggles with any solids.

A

MND (Bulbar onset)

138
Q

What is the diagnosis:

A 61 year old female presents with visual disturbances when moving her eyes. She takes longer to focus than she used to and this irritates her.
On examination her eyes are slow to track your finger but do not fatigue.

A

MND (Ocular onset)

139
Q

What percentage of intracranial tumours are primary brain tumours?

A

10% (90% metastases)

140
Q

What is the incidence of primary brain tumours?

A

14/100,000 per year

141
Q

From what cellular origin are gliomas?

What tumours are gliomas?

A

neuroepithelial origin.

Astrocytic tumours, Oligodendromas, Ependyomas, Choroid plexus papillomas/carcinomas, Pineal parenchymal tumours

142
Q

Other than gliomas, what types of brain tumour are there?

A

Meningiomas (Benign), Heamangioblastomas (blood vessels), Primary CNS Lymphoma (PCNSL), Metastatic tumours (mostly breast and bronchus)

143
Q

What can cause certain types of brain tumours?

A

Cranial irritation can cause meningiomas or astrocytomas
Immunosuppression can cause PCNSL
Von Hippel-Lindau syndrome can cause Heamangioblastomas

144
Q

How do cranial tumours present?

A 
Progressive neurological deficit, mostly with focal signs
Seizures
Raised ICP
Headache
Cognitive and behavioural changes
Weight loss
145
Q

How might you investigate a suspected cranial tumour?

A

CT/MRI head (+angiogram if tumour or aneurysm shown on first scan)
Biopsy

CXR, Mammogram, PET scan, Bone scan, LP - If mets suspected

146
Q

How do you manage intracranial tumours?

A

Surgical resection or debulking, sometimes after watchful waiting

147
Q

Define epilepsy

A

A tendency to experience recurrent epileptic seizures

148
Q

What are the criteria required to diagnose epilepsy?

A

Two definitely epileptic (identical) seizures, or one epileptic seizure with evidence of high risk of another seizure.

149
Q

What can cause epilepsy?

A

Cerebrovascular disease or malformation
Cerebral tumour
Alcohol
Genetics

150
Q

What types of epilepsy exist?

A

Idiopathic:

  • Childhood absence epilepsy
  • Juvenile myoclonic epilepsy
  • Generalised tonic-clonic epilepsy
  • Reading epilepsy (focal)

Structural abnormality (Symptomatic) or Suspected abnormality (Cryptogenic):

  • Myoclonic encepahlopathy
  • West’s sundrome
  • Myoclonic abscence epilepsy
  • Simple or complex partial seizures (focal)
151
Q

If epileptic seizures are triggered, what can be the trigger?

A 
Alcohol
Fatigue
Infection
Hypoglycaemia
Stress
Strobe lighting
152
Q

How do absence seizures present?

A

Brief loss of awareness, occuring frequently
Rare after age 10, more likely in females
Triggered by hyperventillation
No post ictal symptoms

153
Q

How does juvenile myoclonic epilepsy present?

A

Morning myoclonic jerks, onset before 30, can include absence or tonic-clonic seizures
Post ictal confusion/drowsiness

154
Q

How do complex partial seizures present?

A

Associated with structural abnormalities, patients experience Deja Vu and Jamais Vu, unusual behaviour and emotions and frequently stereotypical hand movements and lip smacking
Post ictal confusion/drowsiness

155
Q

How do focal frontal seizures present?

A

Figure 4 sign, maintain consciousness throughout seizure with rapid recovery

156
Q

How do generalised tonic-clonic seizures present?

A

Initial rigidity followed by jerking movements of progressively lower frequency (Hz) but greater movement. Lasting 2-3 mins and frequently involving tongue biting (side), incontinence and post-ictal headache/confusion

157
Q

What investigations would be appropriate for epilepsy?

A

FBC, ESR, U+E, LFT, Ca, glucose, CK
ECG (rule out prolonged PT interval causing T/C seizures)
MRI head
EEG

158
Q

How is epilepsy managed?

A

GTC - Sodium Valporate
Focal - Lamotrigine
Myoclonic - Levetriacetam
JME - Lamotrigine

Driving advice - no driving for 12 months, inform DVLA
Safety advice - Avoid dangerous activities and baths. Protect radiators and open fires.

159
Q

What causes migraines?

A

Impaired cerebral cortical perfusion

160
Q

What proportion of men and women are affected by migraines?

When do they usually start?

A

6% Men, 18% Women

Age of onset 19

161
Q

What are the risk factors for migraines?

A

Family history (70% if both parents, 100% if familial hemiplegic migraine - AD)
Female (can be related to menstrual cycle)
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy)

162
Q

What might trigger a migraine?

A 
Stress
Dehydration
Sleep disturbances
Trauma
Hypoglycaemia
Caffeine
Exercise
Heat
Drugs
163
Q

How does a migraine present?

A

Episodic, mostly unilateral headache with radiations to the neck. Starts dull but builds up to a throbbing nature, worsened by movement. These episodes last over 60 minutes and can be accompanied by nausea, vomiting, photophobia or focal symptoms (eg vertigo/diplopia from brainstem, CNIII paresis from occular muscles, Impaired vision from retina)
Frequently preceded by an aura of a visual, sensory or muscular weakness nature.

164
Q

What is the management for migraines?

A

Analgesia (Paracetamol) - BEWARE analgesia overdose headache -
Antiemetic (Domperidone, Metoclopromide)
Triptans (Rizatriptan or Sumatriptan)

Prophylaxis - Propranolol, Amitryptaline, avoidance of triggers

165
Q

Describe the epidemiology of cluster headaches

A

Prevelance is 0.1%
Males 5x more likely than females
Onset 30-40s

166
Q

What are the symptoms of a cluster headache?

Describe the two types.

A

Periods of frequent headaches (clusters) with periods of remission.
Headaches are severe, unilateral, orbital and supraorbital with temporal pain.
Onset and cessation abrupt.
Associated with lacrimation, nasal congestion, facial sweating, ptosis, conjunctivitis, restlessness and agitation

Episodic - Episodes of 1-52 weeks with over 1 month remission in between
Chronic - Episodes over 52 weeks with less than 1 month remission in between

167
Q

What can trigger cluster headaches?

A

Alcohol
Exercise
GTN

168
Q

How are cluster headaches managed?

A

Acute attack - SC sumatriptan BD, 100% Oxygen non-rebreathe bag, topical lidocaine

Prophylaxis
Short term - prednisolone (60mg then reduce), Methysergide (daily for 5/12, then 1/12 break)
Long term - Verpamil or Lithium

169
Q

What must patients be warned about when treating their own tension headaches?

A

Beware analgesia overuse headache - don’t use aspirin or paracetamol regularly but only when the headache starts

170
Q

What is the prevalence of Parkinson’s?

A

150/100,000

171
Q

What factors modify the risk of contracting Parkinson’s disease?

A

Farming, Pesticides and rural living increases risk

Smoking and caffeine reduce risk

172
Q

Describe the pathophysiology of Parkinson’s disease

A

Caused when dopamine levels drop below 20%.
The substantia nigra produces dopamine, but neuronal cell death or lewy bodies in this area creating loss of more than half of the cell mass leads to reduced dopamine synthesis. This reduces the dopamine supply to the basal gangia causing slowed movements, but also slowing the subthalamic nucleus and hence less of a dampener is applied to movements and so excessive movements can be seen (Chorea or tremor)

173
Q

What are the clinical features of Parkinson’s disease?

A 
Bradykinesia
Hypertonia
Resting tremor
Postural instability
Shuffling gait
Unilateral symptom onset with progression
A good response to levo-dopa treatment

Anosmia
Dystonia
Mild bladder/bowel symptoms

174
Q

What investigations should be completed for ?Parkinson’s disease?

A

NO DIAGNOSTIC TEST
Serum copper if patient is under 50 (?Wilson’s disease)
MRI head
Cognitive assessment, autonomic function test and sphincter EMG (?MSA)

175
Q

What is the management of Parkinson’s disease?

A

Levo-dopa (SE: N+V, anorexia)
Dopamine agonists
MDT - PD nurse, physiotherapy, OT, social worker

Look out for comorbidities - depression, psychosis, dementia, sleep problems, hypersalivation, falls

176
Q

What, aside from Parkinson’s disease, can cause Parkinsonism?

A 
Multi-System Atrophy (MSA)
Progressive Supranuclear Palsy (PSP)
Drugs (Antipsychotics)
Vascular Parkinson's
Hydrocephalus
Alzheimer's
Wilson's
Huntington's
177
Q

Describe MSA

A

Multiple system atrophy
Presents in 60s
Causes atrophy of numerous neurological systems - Striatum, Substantia nigra, Brainstem nuclei, Cerebellum, Onuf’s nucleus (sphincter control)
Anteriomedial spinal cord columns

178
Q

How does MSA present?

A 
Parkinsonism - Akinetic, rigid syndrome
Ataxia
Stridor
Sleep apnoea
Impotence (M) or anorgasmia (F)
Orthostatic hypotension
Incontinence or urgency
179
Q

How is MSA investigated?

A

Autonomic function test

MRI (Hot cross bun sign of pons = intrapontine CSF, cerebellar and peduncular atrophy)

180
Q

How is MSA managed?

A

Levo-dopa
Amantadine (2nd line)

Symptomatic treatment

181
Q

At what age does PSP typically present?

A

60-70s

182
Q

How does PSP present?

A 
Symmetrical akinetic, rigid syndrome with mostly proximal involvement
Downgaze difficulty (reading/walking down stairs)
Eyelid retraction (looks permenantly surprised)
183
Q

How is PSP investigated and what might it show?

A

MRI (T2)

Shows mickey mouse ears (Axial) - midbrain atrophy or hummingbird sign (Sagittal)

184
Q

How is PSP managed?

A

Amantadine
PEG tube if dysphagia
Beware pneumonia (most common cause of death)

185
Q

Describe the epidemiology of carpel tunnel syndrome

A

Median nerve entrapment at the wrist
More likely in females
Peak age 45-54

186
Q

What associations are linked to carpel tunnel syndrome?

A 
Hypothyroid
Rheumatoid disease
Acromegaly
Amyloidosis
3rd trimester of pregnancy
187
Q

What are the clinical features of carpel tunnel syndrome?

A

Paraesthesiae or pain or numbness in thumb and first two fingers of hand (also lateral half of 3rd finger)
Frequently bilateral
Neurological symptoms may extend up to the shoulder
Worse at night or when using hand power
Weak APB (abductor pollicis brevis)
Positive Tinel’s and Phalen’s signs

188
Q

What investigations should be done for carpel tunnel syndrome?

A

TFTs, Glucose, FBC, ESR

NCS and EMG

189
Q

How is carpel tunnel syndrome managed?

A 
Wrist splint
Corticosteroid injection (intracarpal space)
Oral prednisolone (2 weeks)

Surgical release if necessary

190
Q

Describe ulnar nerve compression

A

Entrapment of the ulnar nerve in the cubital tunnel at the elbow

191
Q

Describe the clinical features of ulnar nerve compression

A

Numbness of 4th and 5th digits, initially intermittent
Wasting of first dorsal interosseous muscle, hypothenar eminence and forearm
Claw hand
Elbow Tinnel’s sign positive

192
Q

What can cause ulnar nerve compression?

A

Elbow trauma, fracture or soft tissue injury

193
Q

What investigations are appropriate for ulnar nerve compression? Why?

A

NCT
EMG

Check for involvement of other nerves

194
Q

How is ulnar nerve compression managed?

A

Avoidance of injury or repetitive flexion-extension of elbow (eg hammering)
Surgical release

195
Q

Describe brain abscesses

A

A pus-filled swelling in the brain usually following a bacterial or fungal infection. MEDICAL EMERGENCY

196
Q

What can cause a brain abscess?

A 
Otitis media
Sinusitis
Mastoiditis
Sepsis
Immunosupression
Dental abscess
Head trauma/neurosurgery
197
Q

What are the clinical features of a brain abscess?

A 
Localised, severe headache which is unresponsive to analgesia
Confusion or agitation
Focal neurological signs
Fever
Seizures
Nausea and vomiting
Neck stiffness
198
Q

What investigations are appropriate for ?brain abscess?

A

FBC, CRP, ESR, Cultures
CT/MRI head
CT guided aspiration for MC+S

199
Q

How are brain abscesses managed?

A

IV antibiotics or IV antifungals

If larger than 2cm for aspiration (simple or crainotomy)

200
Q

Name two subtypes of spinal cord compression

A

Cauda equina and Brown-Sequard syndrome

201
Q

What can cause spinal cord compression?

A 
Disc protrusion
Vertebral spondylosis
Spinal trauma
Tumours (Meningioma, Neurofibroma, Mets causing vertebral body collapse)
TB
Spinal epidural abscess or haemorrhage
202
Q

What are the clinical features of spinal cord compression

A

Bilateral pain or sensory disturbance
Bilateral motor disturbance with reflex deficits
Urinary and faecal incontinence
Back pain

Associative symptoms of causative agent

203
Q

What investigations are appropriate for ?spinal cord compression?

A

MRI spine
LP (if MRI clear)
Bladder scan
CT spine if MRI clear

204
Q

What is the treatment of spinal cord compression?

A

Surgical decompression
Steroids
Appropriate treatment of causative agent

205
Q

Describe an extradural haematoma.

What can cause one?

A

An arterial haemorrhage which strips the dura mater off the inner aspect of the skull and hence compresses the brain.

Caused by head injury and skull fracture, most commonly the middle meningeal artery

206
Q

What are the symptoms of an extradural haematoma?

A

Instant loss of consciousness following trauma, followed by a lucid period with later decline in GCS

207
Q

What investigation is recommended in ?extradural haematoma?

What are you likely to see?

A

CT head

Biconvex high-density extradural mass that does not cross cranial sutures.

208
Q

What is the management for extradural haematoma?

A

ABCDE resuscitation
Neurosurgery - burr hole, crainotomy and haematoma excavation.
Beware anticoagulant or antiplatelet therapy

209
Q

What is the prognosis following an extradural haematoma?

A

Good with quick surgical intervention

210
Q

Describe a subdural haematoma

A

Arterial and venous haemorrhage from contused cerebral coretex and cerebral arteries/veins and bridging arteries/veins. Blood is between dura and cerebrum, causing further cortical damage

Follows high impact head injury, especially RTA

211
Q

What are the symptoms of subdural haematoma?

A

Sudden loss of consciousness following trauma, followed by lucid period and slowly reducing GCS
Headache

212
Q

What investigation should be done when ?subdural haematoma

A

CT head
Cresenteric hyperdense mass crossing cranial sutures and into interhemispheric fissure.
NB active bleeding is low density

213
Q

What is the management of subdural haematoma?

A

ABCDE resuscitation
Craniotomy with large flaps for exposing and excavating haemotoma
Postoperative ventilation and ICP monitoring

214
Q

What is the prognosis of subdural haematoma?

A

Mixed, mortality 50%

215
Q

What is the difference between afferent and efferent pathways?

A

Afferent pathways are sensory, such as sensing bright light on the retina
Efferent pathways are motor, such as constricting the pupil

216
Q

What is a Marcus-Gunn pupil?

A

One with a relative afferent pupillary defect (RAPD)
This means the pupil will constrict less when the same light is shone on the affected eye compared to the normal eye. This is seen in the swinging light test

217
Q

Describe horners syndrome on inspection

A

pinpoint pupils

218
Q

What can show irregular findings on eye examination without new pathology?

A

Blind eyes - fixed dilated pupil(s)

Glass eyes - Fixed normal size pupils

219
Q

What can cause unilateral vision loss?

A 
Amaurosis fugax (central retinal artery occusion)
CRVO (central retinal vein occlusion)
Anterior ischaemic optic neuropathy
Giant cell arteritis
Optic neuritis
Retinal detachment
Vitreous haemorrhage
Acute angle closure glaucoma
220
Q

What is dyschromatopsia?

A

Inability to perceive colours

221
Q

Describe optic neuritis

A

Reduced visual acuity over a few days with pain and dyschromatopsia. Caused by inflammation of the optic nerve.

222
Q

What can cause optic neuritis?

A 
MS
Infection (Lymes, Syphilis, HIV, Shingles)
B12 defficiency
Arteritis
Drugs (Ethanbutol and Isoniazid)
223
Q

How is optic neuritis treated?

A

Steroids

224
Q

Describe the four presentations of MS

A

Primary progressive - steady decline in function
Relapsing remitting - periods of stability inter-spaced with relapses from which recovery is rarely complete
Secondary progressive - initially relapsing remitting then becomes progressive after a period of that
Benign - relapses from which recovery is always complete

225
Q

How is the first MS attack described?

A

A clinically isolated syndrome - diagnosis requires multiple CNS lesions causing symptoms that last over 24 hours and affect separate body parts

226
Q

What are the features of MS?

A 
Optic neuritis
Pyramidal weakness and spastic paraparesis
Sensory disturbance
Cerebellar symptoms
Bladder symptoms 
Sexual dysfunction
Fatigue
Cognitive impairment
Lhermitte's phenomenon
Uhtoff's phenomenon
227
Q

What is Lhermitte’s phenomenon?

A

Electric shock sensation sent down spine all the way to fingers and toes, caused by neck flexion

228
Q

What is Unthoff’s phenomenon?

A

Worsening of symptoms in heat (fever, bath, exercise)

229
Q

What investigations are appropriate for MS?

A

MRI head (paraventricular lesions in white matter on T2)
LP (oligoclonal bands)
Visually evoked potentials (abnormal findings - slow transmission)

230
Q

What is the management of MS?

A 
Steroids
Disease modifying treatments - Beta interferon and MABs (Natalizumab)
Stem cell transplant (if under 46)
Physiotherapy
MS specialist nurse
Gabapentin
Clonazepam
Botox if required
231
Q

Define syncope

A

Abrupt and transient loss of consciousness and postural tone due to sudden fall in cerebral perfusion

232
Q

What can cause syncope?

A 
Neurogenic (inappropriate activation of cardioinhibitory and vasodepressor reflex)
Vasovagal
Reflex (eg cough or micturation)
Carotid sinus hypersensativity
Orthostatic
Cardiac
233
Q

What can trigger a syncopal episode?

A 
Stress
Fear
Prolonged standing
Heat
Venepuncture
Reflexes
234
Q

Describe a syncopal episode

A 
Acute onset with prodrome, preventable at this point if patient sits or lays down
Duration less than one minute
Rarely involves convulsions
Pallor
Quick recovery with little confusion
235
Q

When is a CHADs2VASc score completed?

A

When a patient has AF - assess the risk of a stroke. Score over 1 suggests use of Warfarin/NOAC

236
Q

When is a HasBled score used?

A

When prescribing anticoagulation to a patient - risk of a major bleed. If over 3 use caution

Phase 3A DJF (3 decks)

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