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Y4 Special senses > Neurology > Flashcards

Neurology Flashcards

1
Q

Clinical presentation of SOC

A
  • Seizures- (common with temporal lobe lesions) aura, cortical sensors are located in the temporal lobes
  • Focal neurology and gait disturbance
    RIP
  • Headaches
  • Vomiting
  • Papilloedema

Neuropsychiatric effects
- Personality (frontal lobe tumours)
- Mental state
- Memory and cognition
Incidental finding on imaging

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2
Q

Imaging for SOL

A

CT with or without contrast
MRI (usually done with contrast) egfr >30, no allergy to contrast
Diffusion weighted MRI

Contrast- areas of vascularity are more priminent, helpful if tumoru ro infection suspected

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3
Q

What is multi-modal MRI

A

MR spectroscopy (to assess metabolism)
MR perfusion (to assess vascularity)

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4
Q

How to describe the MRI/CT

A

Particularly
Interesting
Surgeons
Love
Carefully
Drilling
Massive
Burr
Holes

Patient and imaging technique details
Intra or extra-axial
Shape (irregular,circular)
Location
- Supra or infratentorial
- Lobes/parts of brain involved
Density OR intensity
- Hypo/hyperdense used with CT
- Hypo/hyperintense used with MRI (how white the lesion)
Border
- How defined
- Oedema
Contrast enhancement
- Homogenous/heterogenous
- Rim enhancemnet
Mass effect
- Effacement of sulci; ipsilateral/contralateral
- Midline shift
- Ventricle compression
- Basal cisterns: obliterated/patent
- Hydrocephalus

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5
Q

Differential diagnosis for intracranial mass lesions

A

Vascular
- Haemorrhage
- Infarct
- Vascular malformation
- Aneurysm

Infection
- Abscess

Neoplastic
- Metastasis
- Primary brain tumours

Cyst

Inflammatory
- Multiple sclerosis
- Granulomatous disease

(Google images of SOL on CT and MRI)

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6
Q

What is the standard investigation within neurology?

A

Non contrast CT followed by MRI is standard investigation

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7
Q

Aetiology of cord compression

A
  • Trauma
  • Prolapsed intervertebral disc
  • Atlantoaxial subluxation
  • Infection
  • Bone metastases
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8
Q

What is paraplegia? (below T1)

A

Partial or total paralysis in the lower half of the body
Including the legs, feet and toes

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9
Q

What is tetraplegia (above T1)

A

Severe form of paralysis that affects all four limbs, the trunk, and the pelvic organs

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10
Q

What are red flag symptoms of spinal cord compression

A
  • Weakness
  • Paraesthesia
  • Ataxia
  • Urinary retention
  • UMN signs (clonus, hyperreflfexia)
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11
Q

How common is it for herniated lumbar discs to cause spinal cord compression?

A

2%

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12
Q

Most common location for prolapse

A

L4/L5 or L5/S1 intervertebral discs

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13
Q

CES-I

A

Incomplete
Urinary disturbance (reduced urinary sensation
Can’t stream
Loss of desire to void

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14
Q

CES-R

A

Compression has been significant enough to cause retention
Overflow incontinence

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15
Q

CES requires what for diagnosis

A

Saddle paraesthesia and impairment of bladder, bowel and sexual function

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16
Q

What are the other symptoms of CES that present more inconsistently

A
  • Loss of lower limb reflexes
  • Loss of anal tone
  • Lower limb weakness and sensory deficit, which is often asymmetrical
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17
Q

Investigations and management for CE

A

Emergency MRI of the lumbar spine
Urgent referral to neurosurgical department
Surgical decompression within 48 hours of onset of symptoms

Metastatic disease- radiotherapy
Ankylosing spondylitis- steroids
Infective like discitis- long term antibiotics

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18
Q

Characteristics of true epileptic fits

A
  • Biting the tongue
  • Incontinence (but can occur in syncope)
  • Eyes open (normally closed in syncope)
  • Last around 2-4 minutes
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19
Q

Is epilepsy more common in people with learning disabilities?

A

Yes
‘Bad epilepsy occurs in bad brains’

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20
Q

Some common causes of learning disabilities where epilepsy is prevalent?

A

Tuberous sclerosis= epilepsy is about 90%

Fragile X syndrome= epilepsy is about 20%

Down syndrome= epilepsy is about 10%

Fetal alcohol syndrome= epilepsy is about 10%

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21
Q

Difference between seizure and epilepsy?

A

Seizure is the event

Epilepsy is the disease associated with spontaneously recurring seizures

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22
Q

Causes of seizures that aren’t epilepsy

A
  • Febrile seizures in children aged 6 months to 6 years
  • Alcohol withdrawal seizures
  • Metabolic seizures (sodium, calcium, magnesium, glucose and oxygen)
  • Toxic seizures
  • Convulsive syncope
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23
Q

What is juvenile myoclonic epilepsy?

A

50% start with typical absences
Followed by frequent myoclonic jerks in the first hour after waking
Then generalised tonic-clonic seizures preceded by run of myoclonic jerks

Excellent response to valproate, levetiracetam

Carbamazepine and phenytoin make fits worse

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24
Q

What is Jamais vu?

A

Oppostive to deja vu
Feeling of unfamiliarity

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25
Q

Typical features of temporal lobe seizures

A

May occur with or without impairment of consciousness or awareness

An aura occurs in most patients
typically a rising epigastric sensation
also psychic or experiential phenomena, such as dejà vu, jamais vu
less commonly hallucinations (auditory/gustatory/olfactory)

Seizures typically last around one minute
automatisms (e.g. lip smacking/grabbing/plucking) are common

Lamotrigine is first choice drug

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26
Q

Common features of frontal lobe seizures

A

Head/leg movements, posturing, post-ictal weakness, Jacksonian march
Bizarre
Often noisy

MRI imaging is indicated

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27
Q

What are opercular seizures?

A
  • Affects the ‘lid of the brain’
  • Homonculus over the lips and mouth
  • Mastication
  • Salivation
  • Swallowing
  • Speech arrest
  • Fear
  • Epigastric aura (hunger, nausea)
  • Gustatory hallucinations (false perceptions of taste, sweet, sour, bitter, salty)
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28
Q

What is Lennox-Gastaut syndrome

A
  • Multiple seizure types- frequent and resistant to treatment
  • Tonic seizures during sleep, drop attacks and atypical absences are common
  • Usually associated with learning disability

EEG is non-specific

First line- valproate
Second line- lamotrigine

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29
Q

Dravet syndrome

A

Appears during first year of life
Seizures may be unilateral (hemiclonic) and prolonged
Other seizure types appear including myoclonic and complex partial
Seizures may be precipitated by heat or pyrexia
Development initially normal, then slows
Balance impairment, ataxia

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30
Q

How do you treat Dravet syndrome?

A

First line- valproate, clobazam
Second line- stiripentol, topiramate

Ketogenic diet and vagus nerve stimulation can be used
Avoid drugs that act on the sodium channels (carbamazepine, phenytoin)

Other such as (gabapentin, pregabalin)

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31
Q

What drugs could provoke abscence status?

A

Tiagabine and vigabatrin

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32
Q

What drugs can make myoclonic epilepsy worse?

A

Carbamazepine and phenyotin

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33
Q

What should gabapentin and pregabalin be avoided in?

A

Abscences and myoclonic jerks worse

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34
Q

If a visual field defect is NOT homonymous, where can it NOT originate from?

A

Anything after the optic chiasm
(Bitemporal hemianopia)
The optic tract, optic radiations of visual cortex

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35
Q

If a bitemporal hemianopia is present, what questions should you be asking in the history?

A
  • Questions relevant to the endocrine status

Think what is close to the optic chiasm! Pituitary gland (sits just behind the optic chiasm), cavernous sinus.

  • Changes in appearance (acromegaly), hat/glove size?
  • Any cold intolerance, lack of energy, menorrhagia (hypothyroidism)
  • Any lactation (prolactin excess)
  • Oligomenorrhoea or amenorrhoea (FSH/LH deficiency)
  • Any weight gain, abdominal striae (ACTH excess)
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36
Q

What can cause an altitudinal field defect (affects upper and lower)

A

Retinal or optic nerve disease
(Think about GCA)

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37
Q

Four common causes of unequal pupils

A
  • 3rd nerve palsy
  • Horner’s syndrome
  • Tonic pupil
  • Pharmacological pupil
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38
Q

What is the main difference between monocular and binocular double vision?

A

Monocular is mainly an optical problem
Binocular is neurological

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39
Q

Sign of congenital horner’s syndrome?

A

Loss of sympathetic innervation
Which stimulates melanocytes
Paler pigment

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40
Q

Is pupil dilation sympathetic or parasympathetic?

A

Sympathetic
Fight or flight- need to allow more light to get into the eyes
Improving vision and awareness

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41
Q

Why do your pupils dilate when you see something you love or find exciting?

A
  • Positive emotions stimulate the sympathetic nervous system ‘similar to fight or flight’
  • Pay more attention
  • Non-verbal social sign, potentially making someone appear more appealing to others
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42
Q

Basic algorithm for seizure management

A

A-E

IV Lorazepam 4mg

Wait 10-15 minutes

IV Lorazepam 4mg

Once established status

Phenytoin infusion 20mg/kg-max rate 50mg/min

Call ITU (patient is not oxygenating while they are seizing- risk of hypoxic brain injury)

Rapid sequence induction-Thiopental

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43
Q

What to do when the seizure terminates

A
  • Close monitoring
  • Await blood results
  • Investigate underlying cause
  • Pabrinex (alcoholism)
  • Collateral history
  • CT head, blood cultures, blood alcohol level, examine for meningism, LP?
  • Contact neurology in morning if remains stable
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44
Q

Definition of a stroke

A

Clinical syndrome consisting of rapidly developing clinical signs of focal or global disturbance of cerebral function
Lasting more than 24 hours
OR lreading to death

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45
Q

Investigations for stroke in all patients

A
  • CT (to see whether it is hemorrhagic or not) or MRI
  • ECG
  • FBC, PT, INR, APTT
  • Electrolytes, blood glucose
  • CRP
  • LFTs, Us&Es
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46
Q

How do you manage a hemorrhagic stroke

A

Neuro intensive care unit

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47
Q

Definition of status epilepticus?

A

A medical emergency where a person has a seizure lasting longer than 5 minutes or mul

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48
Q

Refractory status epilepticus

A

Persisting despite administration of at least 2 appropriately medications

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49
Q

Super refractory status epilepticus

A

Continues for more than 24 hours

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50
Q

Prolonged super refractory status epilepticus

A

Persists more than 7 days

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51
Q

NORSE

A

New onset refractory status epilepticus

No history of prior epilepsy

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52
Q

FIRES

A

Febrile infection related epilepsy syndrome (category of NORSE)

Requires a febrile infection between two weeks and 24-hr prior to the start of refractory status epilepticus

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53
Q

Causes of NORSE

A
  • Infection
  • Cryptogenic
  • Autoimmune
  • FIRES
  • Super-refractory status epileptics of unknown cause
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54
Q

After what time frame of status epilepticus will it become life threatening?

A

30 minutes of a continuous seizure
After this time- we have to completely anesthetize this patient
Intubate the patient, take to ITU for continuous EEG monitoring

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55
Q

Difference between seizure, epilepsy and status epilepticus

A

Seizure= a single episode of abnormal brain activity

Epilepsy= a long-term condition with recurrent, unprovoked seizures

Status epilepticus= A prolonged seizure (more than 5 minutes) requiring urgent medical attention

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56
Q

Initial medical treatment in status epilepticus

A
  • Levertiracetam is started at the same time Lorazepam is
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57
Q

How to assess bulbar reflex

A

Cough

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58
Q

How to assess diaphgram

A

Sniff reflex

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59
Q

Triggers of GBS

A

Infections- Campylobacter, CMV, Zika, HIV, COVID, influenza A and B
Vaccination
Surgery
Trauma
Medications- Isotretinoin, Tacrolimus

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60
Q

Simply explain the pathogenesis of GBS

A

Immune system triggered by infection
- Infection from campylobacter
- Triggers the immune system to produce antibodies to fight the pathogens

Molecular mimicry
- Bacterial/viral proteins share similarities with proteins on nerve cells
- Immune system mistakenly attacks the body’s own nerve cells

Nerve damage and symptoms
- The immune system attacks the myelin
- Muscle weakness, numbness and paralysis

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61
Q

Features needed for diagnosis of Guillain-Barre syndrome in clinical practice

A

Progressive weakness in legs and arms

Areflexia

Progressive phase lasts days to 4 weeks
Relative symmetry
Mild sensory symptoms or signs
Cranial nerve involvement (bilateral weakness of facial muscles)
Pain (common)

IF there is bowel/bladder dysfunction- more likely spinal cord. GBS is peripheral nerves

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62
Q

Explain simply what albuminocytogenic dissociation is?

A

When there is elevated albumin in the CSF while white blood cells are normal

Sign of disruption of blood-brain barrier (inflammation/infection) allows larger molecules to cross into the CSF

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63
Q

What is a myasthenic gravis crisis?

A

Myasthenic crisis is a complication of myasthenia gravis characterized by worsening of muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation.

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64
Q

Features of myasthenia gravis?

A

The key feature of weakness in patients with myasthenia gravis is fatigability.

Patients with myasthenia gravis commonly present with:

Fatiguable limb muscle weakness
Ptosis
Diplopia
Facial palsy
Bulbar weakness e.g. dysphagia, dysphonia
Proximal muscle weakness

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65
Q

ICE pack test for myasthenia

A

> 2mm improvement in ptosis- patient has myasthenia gravis

Cold temperatures- acetylcholinesterase enzyme reduces

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66
Q

Specific test for myasthenia gravis

A

Single fibre EMG will show increased jitter

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67
Q

Treatment for drug-resistant MG

A

Rituximab
Cyclophosphamide
Tacrolimus

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68
Q

Difference between encephalitis and meningitis

A

Encephalitis
- Person of any age, at any time of the year which an acute onset of fever and either a change in mental status (confusion, disorientation, coma or inability to talk)

Or new onset of seizure

Meningitis
- Patient with a history of fever and one of the following signs: neck stiffness, altered consciousness or other meningeal signs

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69
Q

What is jolt accentuation of headache with meningeal irritaiton?

A

Patient rotates his/her head horizontally two to three times per second.

The test is positive if the patient reports exacerbation of his/her headache with this maneuver.

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70
Q

Jerking with syncope

A

Not a seizure

  • Not symmetrical
  • Floppy jerking
  • Eyes roll back
  • Often make a lot of noise

Processes instantly after

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71
Q

Tonic/clonic

A

Tonic- all muscles tighten really quickly- diaphragm tightens and a cry is let out

Clonic- jerking

Clench teeth- snorting, foaming at the mouth, biting tongue

After people won’t remember who they are, where they are, wake up on a different planet

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72
Q

What skeletal muscle groups can myasthenia gravis affect?

A

Extraocular muscles – commonest presentation
Bulbar involvement – dysphagia, dysphonia, dysarthria
Limb weakness – proximal symmetric
Respiratory muscle involvement

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73
Q

What is bulbar palsy?

A

Tongue - weak and wasted and sits in the mouth with fasciculations. Drooling - as saliva collects in the mouth and the patient is unable to swallow (dysphagia). Absent palatal movements. Dysphonia - a rasping tone due to vocal cord paralysis; a nasal tone if bilateral palatal paralysis.

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74
Q

Combination of bulbar and ptosis?

A

Myasthenia until proven otherwise

Why is it not brainstem? Wouldn’t be able to do anything- absolutely bed bound

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75
Q

What can myasthenia gravis be precipitated by?

A

Emotional stress
Pregnancy
Menses
Secondary illness
Thyroid dysfunction
Trauma
Temperature extremes
Hypokalemia
Drugs
Surgery

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76
Q

Tensilon test

A

Acetylcholine receptor inhibitor

See whether it improves the condition

Have to have a cardiac monitor on- can cause asystole

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77
Q

Characteristics of myasthenic crisis and how a cholinergic crisis differs

A

Slack facial muscles
Weak neck- can be resting their head on their breastbone
Drooling
Nasal speech
Generally weak
Unsafe swallow

Cholinergic crisis
Looks similar to myasthenic crisis.
Excess of acetylcholinesterase inhibitors
excessive stimulation of striated muscle - flaccid paralysis
Respiratory failure
Miosis and the SSLUDGE syndrome
(ie, salivation, sweating, lacrimation, urinary incontinence, diarrhea, GI upset and hypermotility, emesis) also may mark cholinergic crisis-not inevitably present

78
Q

Complications of myasthenia gravis

A

Respiratory
Respiratory failure
Aspiration
Respiratory infection

DVT
Thromboprophylaxis

79
Q

Therapeutic management of myasthenia gravis

A

Anticholinesterase inhibitors-
Pyridostigmine- people can take too many of these because they feel so good! Can lead to a cholinergic crisis
Onset 30min; peak 60-120min; duration 3-6hr (need to know this!! Affects swallowing you need to make sure they are given this before they eat!! at peak time, not when the tablet is wearing off
Neostigmine (ITU)

Corticosteroids
Start low – high dose may paradoxically worsen symptoms

Azathioprine
Steroid sparing

IV immunoglobulin
Acute decline or crisis – 60% will respond after 7-10 days

Plasmapheresis- removes AChR antibodies ->short-term improvement
Similar efficacy to IV Ig

80
Q

Early management of myasthenia gravis

A

Supportive measures

Bedside spirometry
FVC (anything else is not sensitive enough) don’t do sats, ABG
If falling or FVC< 18-20ml/kg review as may need ventilation
Blood gases ↑CO2 ↓O2 acidosis late manifestations of type II respiratory failure

No problem with gas exchange- need power! Can’t move air in and out

81
Q

Different subtypes of GBS

A

AIDP – acute inflammatory demyelinating polyradiculoneuropathy – commonest 95% (better recovery)

AMAN – acute motor axonal neuropathy
AMSAN – acute motor and sensory axonal neuropathy
Acute pandysautonomia- every time they move their head, blood pressure drops and can’t get out of bed

Axonal- a lot more difficult to regenerate.

Overlap – Miller Fisher (sensory ataxia, arreflexia, opthalmoplegia)

82
Q

Guillain-Barre pathophsiology

A

1 to 3 weeks after immune system stimulation:
URTI or GI infection
Also: trauma, surgery, vaccination, pregnancy, other

Cross-reaction with schwann cell/ (axolemma) antigens
T-cell sensitization damaging
Myelin
(Axon)

Impaired neurotransmission to the periphery

83
Q

Diagnostic criteria for ‘typical’ GBS

A

Symmetrical length dependent neuropathy (affects the longest nerves first)

Might get ileus- loss of bladder control

Required features:
Progressive weakness in both arms and legs
Areflexia (or hyporeflexia)

Features supportive of diagnosis
Progression of symptoms over days to 4 weeks
Relatively symmetric
Mild sensory signs or symptoms
CN involvement, especially bilateral facial weakness
Recovery begins 2-4 weeks after progression ceases
Autonomic dysfunction
Absence of fever at onset
Typical CSF and EMG/NCS- nerve conduction studies features. Everything might be normal in the first weeks

Don’t let a little detail put you off a diagnosis

84
Q

Diagnostic studies for GBS

A

EMG/ NCS
CSF
↑protein, N/ mild lymphocytes
Increase in protein takes 1-2 weeks to develop
Consider serology
Campylobacter if GI upset
CMV, EBV,HSV,HIV, mycoplasma
Stool cultures
Throat swab

Anti-ganglioside antibodies
AMAN – anti GM1, C Jejuni
MF – anti GQ1B

85
Q

Complications

A
  • Pain- natural spinal curvatures are starting to sag, MSK pain
  • DVT/PE
  • SIADH (forget)
  • Renal failure
  • Hypercalcaemia
86
Q

How to generally manage GBS

A

Close observation as weakness is progressive- can change in the day! riding bike in the morning, ventilator in the evening
Bedside spirometry
Ventilatory support
ECG +/- cardiac monitoring
Nutritional support +/- NG tube
DVT prophylaxis
May need urinary catheter
Laxatives and bowel care
Pain control

87
Q

Severe GBS management

A

IV immunoglobin
Plasmapheresis used within the first 2 weeks of onset. After three weeks, plasmapharesis no benefit
NB steroids not effective

88
Q

What is the complete recovery at 1 year?

A

70%
Not guaranteeing everything but most people do

89
Q

When should you call an ambulance with a seizure?

A
  • Known first tonic-clonic seizure
  • Lasts more than 5 minutes
  • One tonic-clonic seizure after another without gaining consciousness
  • Person becomes injured during the seizure
  • Trouble breathing after their seizur3
90
Q

How does Lorazepam work in a seizure?

A

Lorazepam is a benzodiazepine, a class of drugs that enhances the effect of GABA (a major inhibitory neurotransmitter in the brain).
GABA binds to its receptors and slows down or reduces the activity of nerve cells (neurons).

During a seizure, there is excessive neuronal firing, leading to
uncontrolled brain activity.

Lorazepam increases GABA’s effect, which inhibits the overactive neurons.

This calms the brain’s electrical activity, helping to stop or prevent the seizure.

91
Q

How long do tonic-clonic seizures normally last for?

A

1-3 minutes

92
Q

What is an EMG?

A

An Electromyography (EMG) is a test that checks how well your muscles and the nerves that control them are working. It measures the tiny electrical signals your muscles make when they are active and when they are resting.

93
Q

What is functional overlay?

A

Functional symptoms are real, physical symptoms that cannot be explained by structural damage or a specific disease. They are often associated with stress, anxiety, or emotional factors.

94
Q

How often are MDTs for stroke?

A

5 days a week

95
Q

What do you have to measure in the blood before you give Azathioprine?

A

TMPT
Breaks down thioprine drugs
Can cause

Bone Marrow Suppression (Myelosuppression): The most severe side effect. It can result in:
Leukopenia (low white blood cells), increasing the risk of infections.
Thrombocytopenia (low platelets), leading to increased bleeding risk.
Anemia (low red blood cells), causing fatigue and weakness.
Severe Toxicity: Patients with very low or absent TPMT activity can experience life-threatening toxicity after standard doses of azathioprine, including severe infections or bleeding due to bone marrow failure.

96
Q

What is spinocerebellar ataxia and what is it’s inheritance pattern?

A

Definition: SCA refers to a group of inherited genetic disorders that cause progressive ataxia (loss of coordination and balance) due to the degeneration of the cerebellum (the part of the brain that controls movement) and sometimes the spinal cord or other parts of the brain.
Symptoms:
Difficulty with balance and coordination.
Unsteady walking (gait).
Trouble with fine motor tasks (writing, buttoning clothes).
Slurred speech.
Eye movement abnormalities.
In more severe cases, swallowing and speech can also be affected.

Autosomal dominant

97
Q

What FVC would warrant ITU and what FVC is normal for myasthenia gravis patients?

A

<1= ITU

> 2 is normal

98
Q

How long does Azathioprine take to work?

A

6 months

99
Q

What drugs are used for myasthenia gravis?

A
  1. Azathioprine
  2. Mycophenolate moftil
  3. Rituximab
  4. Cyclophosphamide
100
Q

How long is IVIG given for in a myasthenia gravis crisis?

A

5 days

101
Q

Possible complication of pyridostigmine?

A

Cholinergic crisis

  • Excessive salivation (drooling).
    Lacrimation (excessive tearing).
    Bradycardia (slow heart rate).
    Hypotension (low blood pressure).
    Diarrhea.
    Increased bronchial secretions and bronchospasm (difficulty breathing).
    Miosis (constricted pupils).
    Abdominal cramping.
    Increased sweating.
102
Q

What are the three types of anti-bodies seen in myasthenia gravis?

A
  • Acetylcholine receptor antibodies
  • Muscle specific kinase (MuSK)
  • Low-density lipoproteins receptor related protein 4
103
Q

Why are the muscles of facial expression/eating particularly affected in myasthenia gravis?

A

Fine Motor Control: The facial muscles are responsible for complex movements, such as speaking, eating, and expressing emotions. These muscles require precise neuromuscular transmission and coordination, making them particularly vulnerable to disruptions.

104
Q

What are the most common initial presentations for multiple sclerosis?

A
  • Optic neuritis
  • Transverse myelitis
  • Cerebellar-related symptoms
  • Brainstem syndromes
105
Q

Explain simply what dissemination in space vs time means in the mcdonald criteria for multiple sclerosis?

A

Dissemination in Space: This means that the lesions are found in different areas of the central nervous system (CNS).

Dissemination in Time: This means that the lesions are not all from one single attack but have occurred at different times. This shows that the disease is ongoing. On MRI, this can be shown by finding both “old” and “new” lesions (e.g., a 4-week-old lesion might be older compared to a newer one).- use contrast

106
Q

Differential diagnoses for multiple sclerosis

A
  • Vitamin B12 deficiency
  • HIV
  • Ischaemic stroke
  • Idiopathic transverse myelitis
107
Q

MRI of multiple sclerosis

A

Central nervous system- where the plaques occur in multiple sclerosis- juxta-cortical, next to the cortex
Dawsons’ fingers- from the ventricles
Optic nerve susceptible

108
Q

What can occur if the MLF (medial longitudinal fasciculus) goes wrong

A

Inter-nuclear opthalmoplegia

109
Q

Types of multiple sclerosis

A
  • Relapsing-remitting (85% of patients, young women)
  • Primary progressive
110
Q

Medications used for multiple sclerosis

A
  • Natalizumab (can get GCC virus)
  • Ocrelizumab
  • Fingolumid

Side effects
- Malignancies
- Autoimmune conditions

111
Q

Motor weakness of right arm and sensory loss of left arm

A
  • Spinal cord level
  • Around C7
112
Q

What causes tremors

A
  • Metoclopramide (extra-pyradimal effects)
  • Drug induced (salbutamol)
  • Alcohol withdrawal
  • Benign essential tremor
113
Q

What do you need to make a diagnosis of parkinson’s

A

Bradykinesia

114
Q

What gait is seen in duchenns?

A

Waddling- can’t pick up their hips

115
Q

What does a festinating gait mean?

A

Can’t initiate movement
Visual triggers- can start movement
May need a finger at the back of the head to get them walking- move up from the chair

116
Q

What is the difference between vision changes in multiple sclerosis and myasthenia gravis?

A

Multiple sclerosis
- Blurring of vision due to optic nerve damage
- Loss of colour vision
- Or temporary vision loss in one eye
- Can lead to double vision

Myasthenia
- Double vision
- Ptosis

117
Q

What is the next step when you think someone has a pure peripheral nerve entrapment?

A

Referral to neurophysiology

118
Q

If you think someone has a disc problem, what is the next step?

A

MRI of the relevant body part

119
Q

What do you do if you are not sure whether the lesion is peripheral/nerve root?

A

Neurophysiology and an MRI scan

120
Q

What is meant by the terms primary headache and secondary headache?

A

Primary headache= migraine, tension type headache, cluster headache and other rarer trigemino-autonomic cephalgias

Secondary headaches- headaches caused by a separate underlying pathological process that may be amenable to treatment

121
Q

Possible causes of headache for a man with nausea, vomiting, and photophobia

A

Primary; migraine

Secondary: hangover, meningitis, viral infection, subarachnoid haemorrahge

122
Q

Possible causes of headache for a man with nausea, vomiting, and photophobia

A

Primary; migraine

Secondary: hangover, meningitis, viral infection, subarachnoid haemorrahge

123
Q

List as many causes of secondary headache as you can

A
  • Viral infection
  • Meningitis/Encephalitis
  • Malignancy
  • Abscess
  • Subarachnoid hemorrhage
  • Toxins
  • Glaucoma
  • Sinus disease
  • Metabolic
124
Q

Red flags of headaches

A

Thunderclap headache
Meningism- neck stiffness and photophobia, non-blanching purpuric rash- meningococcal septicaemia
Fever- meningitis/encephalitis, seizures, confusion
RIP- worse in morning, lying down, nausea, vomiting, confusion, cognitive slowing, diplopia, papilloedema (could be a chiari malformation)
Recent onset or change in character- could indicate secondary
Temporal arteritis- jaw claudication, scalp tenderness, headache over temple, redness/swelling-

125
Q

What is the glasgow coma scale?

A

Neurological scale- aims to give a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessment.

126
Q

If you are suspecting a subarachnoid hemorrahge and nothing shows up on the CT scan, how would you proceed?

A

Lumbar puncture
The LP should not be performed within the first 12 hours post headache onset

127
Q

Why should a lumbar puncture be delayed to 12 hours after a bleed?

A

The CSF is analysed by spectrophotometry looking for the bilirubin peak.
Bilirubin is a breakdown product of blood produced as the blood breaks down overtime
You need to give it enough time for there to be bilirbin in the blood

128
Q

What are the causes of subarachnoid haemorrhage?

A
  • Berry aneurysms (majority)
  • Arteriovenous malformations
  • Hypertension
129
Q

How do you manage a subarachnoid hemorrhage?

A
  1. Immediate transfer to interventional neuroradiologists who will treat the aneurysm/AVM (try to prevent a re-bleed)
  2. Nimodipine- prevent vasospasm (which could cause infarction)
  3. Maintain hydration and avoid BP >150
  4. Be aware that hydrocephalus can occur- if deterioration occurs- urgent CT head and CSF shunt
130
Q

If you don’t treat a SAH, what will happen?

A

Patient will have a 50% chance of dying- sudden increase in intracranial pressure, destructive toxic effects of blood

131
Q

If you don’t treat a SAH, what will happen?

A

Patient will have a 50% chance of dying- sudden increase in intracranial pressure, destructive toxic effects of blood

132
Q

What are the characteristics of a migraine?

A

A- At least five attacks fulfilling criteria B-D
B- Headache attacks lasting 4-72 hours
C- Headache has at least two of the following four characteristics:
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routine physical activity

D- During headache at least one of the following:
- Nausea/and or vomiting
- Photophobia and phonophobia

E- Not better accounted for by another ICHD-3 diagnosis -

133
Q

Potential triggers for a migraine

A
  • Stress
  • Lack of sleep
  • Illness
  • Strong smells or perfumes
  • Alcohol
  • Dehydration
  • Too much sleep
134
Q

What is the most powerful way to reduce the frequency of migraine headaches?

A

Address the triggers

135
Q

What is analgesic oversed headache and what level of analgesic use constitutes overuse of analgesics?

A

Analgesic overused headache
- Headache occurring on 15 or more days with a pre-existing headache and developed as a consequence of over-using analgesics

What counts as overusing?
- Simple analgesics (aspirin) must be taken for 15 days or more per month
- Triptans/opioids- 10 days or more

the number of days is more important than the dose

136
Q

What parts of the nervous system are responsible for wakefulness?

A

Ascending reticular activating system (RAS) and cortex

137
Q

How is consciousness lost?

A

Problems with RAS
- Intrinsic brainstem dysfunction
- External pressure causing compression of brainstem and disrupting function of RAS

Problems with cortex
- No blood
- Blood no good (hypoglycaemia, hypoxia)
- Electrical (seizure)
- Trauma

138
Q

What is cataplexy?

A

Temporary muscle weakness when you are feeling very strong emotions

139
Q

What is cataplexy?

A

Temporary muscle weakness when you are feeling very strong emotions

140
Q

What are some causes of short-lived loss of consciousness?

A
  • Seizure
  • Vaso-vagal syncope
  • Hypoglycaemia
  • Cataplexy
  • Head injury
141
Q

Why do tonic-clonic seizures cause a raised lactate?

A

Anaerobic metabolism: Intense muscle activity during a tonic-clonic seizure leads to anaerobic metabolism, producing excess lactate.
Hypoxia: Seizures can cause transient hypoxia, increasing lactate due to reduced oxygen supply.
Catecholamine surge: Seizures trigger a stress response, enhancing lactate production through increased glycolysis.

142
Q

Risk factors for meningitis

A
  • Age
  • Immune status
  • Pregnancy
  • Group setting
  • Occupational exposure
  • Travel
143
Q

Most common bacterial causes for meningitis

A
  • Streptococcus pneumoniae
  • Group B streptococcus
  • Neisseria meningitidis
  • Haemophilus influenzae
  • Listeria monocytogenes
144
Q

Most common viral causes of meningitis

A
  • Non-polio enteroviruses
  • Mumps virus
  • Epstein-Barr virus
145
Q

Most common causes of encephalitis?

A

HSV 1
HSV 2
Varicella zoster
Enteroviruses

146
Q

List causes of central vertigo

A
  • Posterior circulation stroke
  • Vertebrobasilar insufficiency
  • Vertebral artery dissection
  • Multiple sclerosis
  • Posterior fossa tumour
  • Vestibular migraine
147
Q

List causes of peripheral vertigo

A
  • BPPV
  • Menieres disease
  • Vestibular neuronitis
  • Vestibular labrynthitis
  • Cholesteatoma
  • Ramsay hunt syndrome
  • Aminoglycosides like gentamicin
148
Q

What are the four things to examine when investigating veritgo?

A
  • Ear examination to look for signs of infection or other pathology
  • Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis)
  • Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease)
  • Special tests: Cerebellar examination, Romberg’s, Dix-Hallpike and HINTS
149
Q

What associated symptoms would go along with a neurological cause of veritgo?

A

Neurological — such as headache, diplopia, visual disturbance, dysarthria or dysphagia, paraesthesia, muscle weakness, ataxia, or migraine aura.

150
Q

What associated symptoms would go along with a otological cause of veritgo?

A

Otological — such as hearing loss, ear discharge, a feeling of fullness in the ear, or tinnitus.

151
Q

What are the three main causes of primary headaches?

A
  • Migraine
  • Tension-type
  • Trigeminal autonomic cephalgias (including cluster headache).
152
Q

What defines acute headaches?

A

Over seconds to hours

153
Q

What defines subacute headaches?

A

Over hours to days

154
Q

What defines chronic headaches?

A

Over weeks to months

155
Q

Causes of acute headaches?

A
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
  • Migraine
  • Trauma (subdural haematoma, extradural haemorrhage)
  • Arterial dissection
156
Q

Causes of subacute headaches

A
  • GCA
  • Brain abscess
  • SOL
  • IIH
157
Q

Causes of chronic headaches

A
  • Tension
  • Migraine
  • Cluster
  • Cervical spondylosis
  • Sinusitis
158
Q

In the brain, what naturally calcifies as you age?

A

Pineal glands

159
Q

What is Susac syndrome?

A

Susac syndrome is a rare autoimmune condition characterized by damage to the small blood vessels in the brain, retina, and inner ear, leading to symptoms such as encephalopathy, vision changes, and hearing loss.

160
Q

What is a flair sequence?

A

A FLAIR (Fluid-Attenuated Inversion Recovery) sequence in MRI is a technique that suppresses fluid signals, enhancing the visibility of lesions near cerebrospinal fluid-filled spaces.

161
Q

What are Dawson’s fingers?

A

Dawson’s fingers are white matter lesions seen on MRI, shaped like elongated ovals radiating perpendicular to the ventricles, typically associated with multiple sclerosis.

162
Q

What would cause a vasogenic oedema?

A

Tumor
Abscess

Vasogenic oedema (would straddle both vascular territories making infarct less likely)

163
Q

What would atrophy of hippocampi look like?

A

The hippocampi are located in the medial temporal lobes, on either side of the brain. Normally, they appear as rounded, protruding “hills” in this area, but with atrophy, they shrink and the surrounding spaces, like the temporal horns of the lateral ventricles, look larger and more prominent.

164
Q

Indications for requesting a CT head

A
  • New focal neurological deficit
  • Seizure
  • Headaches (red flag symptoms)
  • Change in mental status
165
Q

Have a look at hair extensions artefact on CT head

A
166
Q

Have a look at deep brain stimulation leads to treat parkinson’s disease on imaging

A
167
Q

Have a look at ventriculoperitoneal shunts

A
168
Q

Have a look at global hypoxic ischaemic brain injury on head CT

A

-Lack of sulci

169
Q

How can you tell whether a CT head is acute

A

Here’s how you can tell a CT head shows an acute stroke, explained simply:

Loss of Sulci (Sulcal Effacement): The grooves (sulci) on the brain’s surface appear less defined because of swelling.
Oedema (Swelling): Affected brain tissue looks darker (hypodense) compared to surrounding areas because of fluid accumulation.
Loss of Grey-White Differentiation: The boundary between grey and white matter becomes harder to see, particularly in the affected area.
Hyperdense Artery Sign: If a clot is present, the artery (e.g., the middle cerebral artery) may look unusually bright.
Mass Effect: Swelling can push structures, such as ventricles, out of their usual position.

170
Q

What is a contre-coup injury on CT head?

A

When there is head trauma
Injury on the opposite side of the brain

171
Q

What would optic neuritis look like on an MRI?

A

T2 weighted
Optic nerve would appear as bright as the CSF surrounding it.
Inflammation

172
Q

Outline the pathway of the oculomotor nerve

A

Origin
- Motor fibres: oculomotor nucleus (midbrain)
- Parasympathetic fibres: Edinger-Westphal nucleus (midbrain)

Path
- Exits brain via interpeduncular fossa
- Passes between posterior and superior cerebellar arteries
- Enters cavernous sinus (divides into superior and inferior divisions)
- Runs lateral to posterior communicating artery (common site of aneurysm) hence susceptible to posterior communicating artery aneurysm

Orbit
- Passes through superior orbital fissure within the annulus of Zinn
- Divides into:
Superior division= superior rectus, LPS
Inferior division= medial rectus, inferior rectus, inferior oblique and the parasympathetic fibres are sent to the ciliary ganglion

173
Q

Function of the parasympathetic part of the oculomotor nerve

A

Pupil constriction (sphincter pupillae)
Lens accommodation (ciliary muscle)

174
Q

Go over the anatomy at the lateral wall of the cavernous sinus where all the cranial nerves are

A
175
Q

Have a look at ventricles on scans

A
176
Q

What lesion appears as an ice cream cone shape on CT?

A

Vestibular schwannoma (look at photo)

177
Q

What is the difference between pulsatile and non-pulsatile tinnitus?

A

Pulsatile= normally matches the patient’s heartbeat
- Vascular malformations
- Carotid artery stenosis, glomus tumours (highly vascular)

Non-pulsatile= a continuous, non-rhythmic noise that does not correlate with the heartbeat. Ringing, buzzing, hissing or humming
- Auditory
- Presbycusis
- Meniere’s
- Ototoxic drugs (aminoglycosides)

178
Q

What would be the diagnosis with a pulsatile tinnitus

A
179
Q

What part of the optic nerve is affected in temporal arteritis?

A

The anterior part of the optic nerve
Painful
Due to the fact that temporal arteritis usually affects the short posterior ciliary arteries, which supply blood to the anterior optic nerve.

180
Q

What nerves are involved in the corneal reflex?

A

Ophthalmic branch of the trigeminal nerve (CN V1) – Afferent (sensory) limb:

The ophthalmic branch (V1) of the trigeminal nerve is responsible for sensation of the cornea. When the cornea is touched (such as with a wisp of cotton), this branch transmits the sensory information to the brain.
It is the sensory component of the corneal reflex, meaning it detects the stimulus (like touch or irritation) on the cornea.
Temporal branch of the facial nerve (CN VII) – Efferent (motor) limb:

The temporal branch of the facial nerve is responsible for causing the blink response. Once the sensory signal is sent to the brain, the motor response (blinking) is triggered by the facial nerve to contract the orbicularis oculi muscle, which closes the eyelid.
This is the motor component of the corneal reflex.

181
Q

What muscle closes the eyelid?

A

The muscle responsible for closing the eyelid is the orbicularis oculi.

Supplied by the temporal and zygomatic branches of the facial nerve

182
Q

What is an immediate giveaway that there is a brainstem stroke?

A

Crossed findings
Weakness of the face is on the opposite side to weakness on the body

183
Q

How to remember the midline structures of the brainstem?

A

All begin with M

Motor pathway
Medial lemniscus
Medial longitudinal fasciculus
Motor component of cranial nerves

184
Q

How to remember the side structures of the brainstem

A

All begin with S

Spinocerebellary pathway
Spinothalamic pathway
Sensory to the face
Sympathetic pathway

185
Q

What is amaurosis fugax?

A

Amaurosis fugax is a temporary loss of vision in one or both eyes that occurs when blood flow to the retina is disrupted. The term comes from the Greek word amaurosis, meaning “dark”, and the Latin word fugax, meaning “fleeting”

186
Q

What cranial nerves are likely to be at the cerebellopontine angle?

A
  • Vestibulocochlear nerve (hearing loss common in vestibular schwannomas)
  • Facial nerve
187
Q

What causes a weakness of dorsiflexion?

A
  • Peripheral neuropathy or fibular nerve palsy
  • Common in charcot-marie tooth disease, diabetic neuropathy, sciatic nerve injury.
188
Q

What is a cause of a high steppage gait?

A

Weakness in the anterior tibial muscles.
Peroneal nerve palsy, L5 raduculopathy or foot drop.

189
Q

What is internuclear ophthalmoplegia associated with and what is it?

A

It is associated with multiple sclerosis or brainstem strokes

It is damage to the medial longitudinal fasciculus (a structure in the brainstem that coordinates horizontal eye movements).

190
Q

Why do you get dysarthria in cerebellar disorders?

A

The cerebellum co-ordinates speech muscles (larynx, tongue and palate)

191
Q

What should you say to patients after you perform the Epley manoeuvre on them?

A
  • Avoid any position for the next two to three days that causes you vertigo
  • Sleep with three pillows at night

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