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Neuroscience Flashcards

1
Q

What is migraine?

A

Severe, episodic headache that may have a prodrome of focal neurological symptoms (aura) and is associated with systemic disturbance

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2
Q

Recall the medical management of migraine both in the acute setting and for prophylaxis

A

Acute:

  1. Anti-emetic - IV metoclopramide
  2. Analgesia - aspirin, paracetamol, NSAID (NO OPIOIDS)
  3. Triptan (5HT1-R agonist) - sumitriptan

Prophylaxis:
1st line = propranolol (BB) or topiramirate (anticonvulsant)
2nd line = TCA - amitriptyline

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3
Q

When does migraine usually present?

A

Teenager - young adult OR middle age

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4
Q

What are the risk factors for migraine?

A

FHx
Lifestyle - caffeine, stress, lack of sleep
Change in barometric pressure - high altitude/weather changes
Female
Obesity - increases risk of chronic migraine
Habitual snoring
Overuse of headache meds

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5
Q

What are the symptoms of migraine?

A 
Prolonged headache - 4-72h
Episodic/recurrent
Throbbing/pulsating
N+V
Decreased ability to function
Headache worse with activity
Sensitivity to light/smell/noise
Aura
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6
Q

What causes migraine?

A

Brain is hyperexcitable to a variety of stimuli

Neuronal depolarisation is more easily triggered

Genetic

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7
Q

How is migraine diagnosed?

A

Clinically

Any investigations are normal

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8
Q

What are the complications of migraine?

A

Status migrainosus - migraine attack > 72h - ?medication overuse as cause, tx w corticosteroids

Depression
Chronic migraine
Seizures
Migrainous infarction

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9
Q

What is Bell’s palsy?

A

Acute unilateral peripheral facial nerve (CNVII) palsy

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10
Q

How is Bell’s palsy diagnosed?

A

Clinical diagnosis of exclusion

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11
Q

What are the risk factors for Bell’s palsy?

A

Intranasal flu vaccine

Pregnancy

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12
Q

What are the symptoms of Bell’s palsy?

A
  1. Single episode
  2. Unilateral
  3. No constitutional symptoms
  4. Dry eyes
  5. Post-auricular pain
  6. Otalgia
  7. Sometimes sensory disturbances
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13
Q

What are the signs of Bell’s palsy?

A

Acute, unilateral facial palsy, with an o/w normal physical examination

Equal distribution of facial weakness across facial zones

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14
Q

Why does Bell’s palsy affect the whole face?

A

Involves all nerve branches (bc blockade originates proximal to geniculate ganglion, prior to any branching)

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15
Q

What causes Bell’s palsy?

A

Reactivation of HSV-1 within the geniculate ganglion after cellular immune suppression

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16
Q

What is the most common cause of unilateral facial palsy in those over 2?

A

Bell’s palsy

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17
Q

In what age group is Bell’s palsy most common?

A

15-45yo

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18
Q

How is Bell’s palsy managed acutely?

A
  1. Corticosteroid - prednisolone - 60mg OD for 5 days, then daily down 10mg until 0 - start within 72h of onset
  2. Eye protection
    - glasses + artificial tears during day
    - ophthalmic lubricant + eyelid taped shut at night
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19
Q

What is the prognosis for Bell’s palsy?

A

Incomplete paralysis on presentation - 94% fully recover

vs 61% of those with complete paralysis

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20
Q

What is cluster headache?

A

Unilateral headache attacks lasting from 15-180 minutes associated w/autonomic symptoms (parasympathetic hyperactivity and sympathetic hypo-activity)

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21
Q

What are the risk factors for cluster headache?

A 
Male
FHx
Head injury
Smoking
Heavy drinking
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22
Q

What is the most common trigger for cluster headache?

A

Alcohol

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23
Q

What are the signs and symptoms of cluster headache?

A 
Unilateral headache attack
15m-3h
Around 4/day
Excruciating pain
Autonomic: lacrimation, rhinorrhoea, partial Horner's
Agitated - can't sit still
Photophobia + phonophobia
Migrainous aura
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24
Q

Recall the aetiology of cluster headache

A

Idiopathic

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25
Q

How is cluster headache investigated?

A

Brain CT/MRI - normal in primary, abnormal in secondary (tumour, cavernous sinus pathology)

ESR - normal in primary, to exclude GCA in patients > 50

Pituitary function tests - normal, abnormalities –> secondary causes resulting from pituitary adenoma

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26
Q

What is encephalitis?

A

Inflammation of the brain parenchyma associated with neurological dysfunction

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27
Q

Recall the aetiology of encephalitis

A

Mainly viral

Usually HSV-1

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28
Q

What are the risk factors for encephalitis?

A 
Age <1 or >65
Immunodeficiency
Viral infections
Blood/body fluid exposure
Organ transplant
Animal or insect bites
Swimming or diving in warm freshwater or nasal/sinus irrigation
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29
Q

What are the presenting symptoms of encephalitis?

A 
Fever
Rash
Altered mental state - drowsy-coma
Headache
Photophobia
Neck stiffness
Seizure
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30
Q

What are the signs of encephalitis?

A 
Pyrexia
Altered mental state
Focal neurological deficit
Meningismus - headache, photophobia, neck stiffness
Seizures
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31
Q

How is encephalitis investigated?

A 
1. BLOODS
FBC - high lymphocytes
UE - SIADH possible (low Na)
Glucose - compare w CSF glucose
Viral serology
ABG
  1. MRI/CT –> HSV - temporal oedema
    Also exclude mass lesion before LP
  2. LP: high lymphocytes and monocytes + high protein
    Culture/PCR
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32
Q

Why must you do a CT brain before a lumbar puncture in suspected encephalitis?

A

To exclude a mass lesion

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33
Q

What is extradural haemorrhage?

A

Bleeding between the dura mater and the inner surface of the skull

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34
Q

What is subdural haemorrhage?

A

Bleeding into the subdural space (between dura and arachnoid mater)

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35
Q

What is subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space (between arachnoid and pia mater)

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36
Q

What causes subdural haemorrhage?

A

Usually TRAUMA:
Blow to temporal side of head
Ruptures bridging cranial veins

Also:
Rupture of cerebral aneurysm
Rupture of arteriovenous malformation
Cerebral hypotension
Malignancy (rare)
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37
Q

What causes subarachnoid haemorrhage?

A

Traumatic injury OR spontaneous

Spontaneous causes:
Ruptured intracranial aneurysms 70%
Arteriovenous malformation 10%
Unknown aetiology 15%
Rare disorders <5%
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38
Q

What is the classic history for extradural haemorrhage?

A

Head trauma + severe headache

Immediate fluctuating level of consciousness following trauma before appearing lucid (lucid interval) - tiredness, confusion

Rapid deterioration some time following regaining consciousness

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39
Q

What are the earl signs of extradural haemorrhage?

A

Severe headache after trauma, can persist

Initial loss/fluctuance in consciousness - tiredness, confusion

Period of lucidity after initial LOC - lasts 6-8h, but can last days

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40
Q

What investigations must be done for extradural haemorrhage?

A

Urgent non-contrast CT head

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41
Q

What does an extradural haemorrhage look like on CT?

A

Lemon
Biconvex lens
Midline shift
Brain stem herniation

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42
Q

What are the late signs of extradural haemorrhage

A
  1. GCS drops as ICP rises and BS begins to herniate
  2. LOC
  3. Focal neurological deficitis in eyes (CN compression) - blown pupil = fixed dilated ipsilateral pupil
  4. Contralateral hemiparesis, can become bilateral (compression of ipsilateral motor cortex)
  5. UMN signs - positive Babinski’s sign (upgoing toes), hyperreflexia + hypertonia
  6. Cushing’s triad due to raised ICP
  7. Persisting unconsciousness -deep coma and v low GCS
  8. Death - resp arrest
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43
Q

What upper motor neuron signs may you see in EDH?

A

Positive Babinski’s - upgoing toes

Hyperreflexia

Hypertonia - spasticity

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44
Q

What is Cushing’s triad and what causes it?

A

Bradycardia
HTN
Deep/irregular breathing

Raised ICP

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45
Q

What investigation are absolutely contraindicated in EDH and why?

A

Lumbar puncture

Result in drop in CSF pressure

May speed up brain herniation

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46
Q

What investigation are absolutely contraindicated in EDH and why?

A

Lumbar puncture

Result in drop in CSF pressure

May speed up brain herniation

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47
Q

What are the risk factors for subdural haemorrhage?

A

Recent trauma
Coagulopathy
Anticoagulant use
>65yo

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48
Q

What are the presenting symptoms of SDH?

A 
Headache
N+V
Confusion
Irritability
Seizure
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49
Q

What are the signs of SDH?

A

Head trauma - abrasions, lacerations

Low GCS:
Diminished eye response: anisocoria (unequal pupil size) - BS herniation
Diminished verbal response
Diminished motor response

Confusion

Focal neurological signs (much more common in acute)

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50
Q

How is SDH investigated?

A

Urgent non-contrast CT: banana/moon

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51
Q

How is SDH managed initially?

A

Resuscitation and stabilisation of vitals: ABCDE

Senior doctor + neurosurgeon + anaesthetist

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52
Q

What are the complications of SDH

A

Complications result from damage from bleed itself + standard post-op complications from surgical Mx

Neuro deficits
Coma
Seizure
Infection
Recurrent haemorrhage
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53
Q

What are poorer functional outcomes in SDH associated with?

A 
Older age
More serious injury
Lower GCS
Midline shift, multiple parenchymal lesions
Raised ICP
Early need for surgery
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54
Q

How can SDH be classified?

A

Acute <3d

Chronic >21d

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55
Q

How does SDH clinically present?

A 
History of trauma
Older
Alcohol misuse
Child - non-accidental injury
Gradual deterioration (worsening headache and confusion)
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56
Q

How is acute SDH managed once confirmed by non-contrast CT?

A

Bleed <10mm size (midline shift <5mm non-expansile without significant neurological dysfunction):

  1. Admit, observe, monitor + follow-up CT in 2-3wks
  2. Prophylactic antiepileptics - IV phenytoin, phenobarbital or oral/IV levetiracetam
  3. ICP monitoring if GCS is <9
  4. Correct coagulopathies (i.e. vitamin K)
  5. Lower ICP

Bleed w 1+ of following: ≥10mm size; w midline shift >5mm; expansile or significant neurological dysfunction - SURGERY FIRST - decompressive craniectomy

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57
Q

What does the management of acute SDH once confirmed depend on?

A

Size of haemorrhage

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58
Q

How is chronic SDH managed once confirmed?

A
  1. Antiepileptic medication - IV phenytoin, IV phenobarbital, oral/IV levetiracetam
  2. Surgery for symptomatic patients- i.e. burr hole irrigation and drainage, craniotomy
  3. Correct coagulopathy- i.e. with vitamin K
  4. Lower ICP
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59
Q

What are the 3 main ways in which SAH damages the brain?

A
  1. Hypoxia
  2. Raised ICP
  3. Direct cranial injury
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60
Q

What are the risk factors for spontaneous SAH?

A 
HTN
Smoking
FHx
Autosomal dominant polycystic kidney disease
<50yo
Female (1.5x baseline risk)
Black
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61
Q

Compare the pathophysiology of EDH, SDH and SAH

A

EDH: rupture of middle meningeal artery on temporal surface of skull

SDH: rupture of bridging cranial veins

SAH: rupture of a berry aneurysm

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62
Q

How does SAH clinically present?

A

Sudden onset severe headache, reaching max intensity within seconds = thunderclap headache

N+V

Photophobia

Reduced consciousness level

Neck stiffness

Kernig’s sign

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63
Q

What is Kernig’s sign?

A

Patient is supine w hip and knee flexed to 90 degrees

Inability/pain on straightening leg

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64
Q

What causes a positive Kernig’s sign?

A

Irritation of motor nerve roots passing through inflamed meninges as they are under tension

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65
Q

How is SAH investigated?

A

Bloods: FBC, U+Es, coagulation studies (useful prior to LP or surgery)

Urgent plain CT head - blood in SA space or hydrocephalus

CT angiogram - can identify aneurysm

LP - only if SAH suspected but CT clear and no evidence of raised ICP

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66
Q

When is a lumbar puncture necessary in suspected SAH?

A

When CT scan clear and shows no evidence of raised ICP (risk of BS coning)

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67
Q

When must a lumbar puncture be performed in suspected SAH for the results to be reliable?

A

At least 12h after onset of symptoms

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68
Q

What does an LP show in SAH?

A

Xanthochromia
Due to infiltration of blood from haemorrhage

Bilirubin
Oxyhaemoglobin

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69
Q

What is Guillain-Barré syndrome?

A

Acute inflammatory demyelinating polyneuropathy

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70
Q

Recall the aetiology of GBS

A
  • Immune-mediated demyelination of PNS

- Often triggered by Campylobacter infection (or Salmonella) about 2 weeks after infection

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71
Q

What are the risk factors for GBS?

A

Preceding viral illness - gastroenteritis or flu-like weeks before onset
Preceding bacterial infection
Hep E infection
Increasing age

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72
Q

What are the presenting symptoms of GBS?

A
  • Ascending symmetrical muscle weakness/paralysis a few weeks after infection
  • Proximal muscles more affected - trunk, resp, CN VII esp
  • Pain - back, limb
  • Autonomic: sweating, high HR, BP changes, arrhythmia, urinary retention
  • Areflexia
  • Diplopia
  • Slurred speech
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73
Q

What are the signs of GBS?

A
  • Symmetrical muscle weakness/paralysis
  • Proximal muscles
  • Tachycardia
  • Areflexia
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74
Q

How is GBS investigated?

A
  1. ABs: 25% +ve for anti-GM1
  2. NCS: slow conduction
  3. LP - CSF: high protein <5.5g/L; normal WCC
  4. Spirometry to monitor lung function (diaphragm involvement)
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75
Q

What are anti-GM1 antibodies indicative of?

A

Guillain-Barre syndrome

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76
Q

What symptoms make up Horner’s syndrome?

A

Ptosis
Miosis
Anhydrosis

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77
Q

What causes Horner’s syndrome?

A

Disruption of SNS to face

Lesion

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78
Q

Where is the lesion located in Horner’s syndrome?

A

Ipsilateral side of symptoms

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79
Q

What tests are used in Horner’s syndrome?

A

Cocaine eye drops - should block reuptake of post-ganglionic NA –> lack of NA in cleft –> mydriatic failure (no effect)

Paredrine - helps localise cause - if 3rd order neuron intact, amphetamine causes NT vesicle release –> NA into cleft –> mydriasis - if lesion in of 3rd order neuron - no effect - pupil stays constricted

Dilation lag test

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80
Q

How is Horner’s syndrome managed?

A

Depends on location and cause of lesion of tumour

Surgical removal

Radiation and chemotherapy

Genetic counselling if have genetic form

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81
Q

What is Huntington’s disease?

A

An autosomal dominant, slowly progressive, neurodegenerative disorder

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82
Q

When does Huntington’s disease usually appear?

A

Mid-adult life

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83
Q

Recall the aetiology of Huntington’s disease

A

Caused by an expanded CAG repeat at the N-terminus of the gene that codes for the huntingtin protein

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84
Q

What are the symptoms of Huntington’s disease?

A 
Chorea
Personality change
Irritability and impulsivity
Twitching or restlessness
Loss of coordination
Deficit in fine motor coordination
Slowed saccades
Motor impersistence
Impaired tandem walking
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85
Q

What are the signs of Huntington’s disease?

A

Slowed saccades - ask pt to look between your 2 fingers held shoulder width apart - head turning or eye blinking

Motor impersistence - ask pt to protrude tongue or close eyes tightly for 10s - pt struggles to maintain

Deficit in fine motor coordination - tapping finger to thumb quickly - pt slow and irregular tempo

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86
Q

How is Huntington’s disease investigated?

A

Nothing initially - clinical diagnosis

CAG repeat testing can be done later - 40+ CAG repeats on 1 of the 2 alleles = +ve
intermediate result = 36-39 repeats

MRI/CT - evident caudate or striatal atrophy

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87
Q

What eye sign is present in Huntington’s disease?

A

Slowed rapid (saccadic) eye movements

88
Q

What eye sign is present in Huntington’s disease?

A

Slowed rapid (saccadic) eye movements

89
Q

What is hydrocephalus?

A

Excessive accumulation of CSF within the brain

90
Q

What causes hydrocephalus?

A 
Congenital (birth defects):
Aqueductal stenosis
Neural-tube defects
Arachnoid cysts
Dandy-Walker syndrome
Arnold-Chiari malformation
Acquired:
CNS infections
Meningitis
Brain tumours
Head trauma
Toxoplasmosis
SAH or intraparenchymal haemorrhage
91
Q

What are the 3 types of hydrocephalus?

A
  1. Non-communicating/obstructive - impaired CSF flow
  2. Communicating/non-obstructive - impaired reabsorption
  3. Excessive CSF production
92
Q

What are the signs and symptoms of hydrocephalus?

A

Varies with chronicity

Acute dilatation of ventricular system manifests w non-specific S&Ss of raised ICP:

  • Headaches worse in morning
  • Get better sitting upright but eventually become continuous
  • N+V
  • Papilloedema
  • Sleepiness or coma

Chronic dilatation (esp in elderly): insidious onset w Hakim’s triad:

  1. Gait instability
  2. Urinary incontinence
  3. Dementia
93
Q

What is lumbar puncture?

A

A needle is inserted into the spinal canal, most commonly to collect CSF for diagnostic testing

94
Q

What are the indications for an LP?

A
  1. Diagnose CNS diseases eg meningitis, SAH
  2. Inject meds - analgesia, ABx, chemo
  3. Spinal anaesthetic (epidural)
  4. Remove some fluid to reduce pressure in skull or spine
95
Q

What are the possible complications of an LP?

A

Post spinal headache w nausea

Parasthesia in leg during procedure

Spinal/epidural bleeding
Adhesive arachnoiditis
SC trauma

96
Q

What is meningitis?

A

An acute inflammation of the meninges

97
Q

Recall the aetiology of meningitis

A 
Viral/bacterial/fungal/protozoal infection
Drugs - NSAIDs, ABx, IV Igs
Metastasis
Sarcoidosis
SLE
Vasculitis
98
Q

What are the presenting symptoms of meningitis?

A 
Headache
N+V
Photophobia
Neck stiffness
Fever
Rash
99
Q

How is meningitis investigated?

A

LP to get CSF sample

Acute bacterial = low glu, high prot, PMNs

Acute viral = norm glu, norm/high prot, mononuclear cells

Tuberculous - low glu, high prot, mononuclear and PMNs

Fungal = low glu, high prot

Malignant = low glu, high prot, mononuclear cells

Bloods - CRP, FBC, cultures

100
Q

How is meningitis managed?

A

Bacterial:

  • empirical cephalosporin eg cefotaxime
  • corticosteroids eg dexamethasone

Viral: supportive or aciclovir

Fungal: long course high-dose antifungals eg amphotericin B

101
Q

What are the possible complications of meningitis?

A

Deafness
Epilepsy
Hydrocephalus
Cognitive deficits

102
Q

What is the most common cause of meningitis?

A

Viral infection

HSV-1

103
Q

What is the prognosis of meningitis?

A

Untreated, bacterial is almost always fatal

Viral - tends to resolve spontaneously and is rarely fatal

104
Q

What are the risk factors for meningitis?

A 
Infants and young children - enteroviral
Young adults - HSV-1
Older people - HSV-1
Summer and autumn in temperate regions
Exposure to mosquito or tick vector - arboviruses
Unvaccinated for mumps
105
Q

What are the risk factors for meningitis?

A 
Infants and young children - enteroviral
Young adults - HSV-1
Older people - HSV-1
Summer and autumn in temperate regions
Exposure to mosquito or tick vector - arboviruses
Unvaccinated for mumps
106
Q

What is motor neurone disease?

A

A group of neurodegenerative disorders that selectively affect motor neurons

107
Q

What are the 6 types of MND?

A
  1. Amyotrophic lateral sclerosis (ALS)
  2. Progressive bulbar palsy (PBP)
  3. Pseudobulbar palsy
  4. Progressive muscular atrophy (PMA)
  5. Primary lateral sclerosis (PLS)
  6. Monomelic amyotrophy (MMA)
108
Q

What are the symptoms of MND?

A

Come on slowly
Worsen over course of more than 3 months

Muscle cramps
Spasms
Exertional dyspnoea
Orthopnoea
Bulbar symptoms: dysarthria, dysphagia, sialorrhoea
Emotional disturbance + cognitive + behavioural changes

109
Q

What are the signs of MND?

A

LMN findings - muscle wasting, fasciculations, hyporeflexia

UMN findings - hyperreflexia, hypertonia, Babinski’s

110
Q

How is MND investigated?

A

CSF tests - infection or inflammaton

MRI - other cause of UMN signs

EMG + NCS - LMN signs
- EMG - acute + chronic denervation and reinnervation of muscle
NCS - normal

Tissue biopsy (rarely)

111
Q

What would sensation testing in MND show?

A

Normal

Sensation not typically affected

112
Q

What is multiple sclerosis?

A

An inflammatory demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of the central nervous system (brain, spinal cord, and optic nerves) separated in time and space

113
Q

Recall the aetiology of MS

A

Inflammatory and degenerative components that may be triggered by environmental factors in genetically-susceptible individuals

Environmental factors - toxins, viral exposures, sunlight exposures (and its effect on vit D metabolism)

114
Q

What are the risk factors for MS?

A

FHx
Female
Northern hemisphere

115
Q

What are the presenting symptoms of MS?

A
  • Graying/blurring of vision in one eye
  • Pain moving one eye
  • Loss of colour discrimination, esp reds
  • Odd sensations of wet patch/burning/hemibody sensory loss/tingling
  • Gradual onset of muscle weakness that resolves w rest
  • Leg cramping esp PM/driving
  • Fatigue
  • Urinary freq
  • Constipation
  • Imbalance/incoordination
116
Q

What are the signs of MS?

A
  • Spasticity/increased muscle tone
  • Increased deep tendon reflexes, asymmetrical (esp clonus at ankles)
  • Wide-based gait
  • Limb ataxia
  • Foot dragging
  • Lhermitte’s sign - electric shock-like sensations extending down cervical spine radiating to limbs
117
Q

How is MS investigated?

A
  1. MRI brain w contrast - hyperintensities in periventricular white matter
  2. MRI SC - demyelinating lesions
  3. FBC - normal
  4. Metabolic panel - normal
  5. TSH - normal
  6. Vitamin B12 - normal
118
Q

When does MS usually present?

A

20-40yo

119
Q

Describe a tension headache

A

Generalised location - mostly frontal and occipital regions
Bilateral
Non-pulsatile/dull
Episodic or chronic
Rarely disabling or associated w any autonomic phenomena

‘Tight band’ around head

120
Q

What are the risk factors for tension headache?

A

Mental tension
Stress
Missing meals
Fatigue

121
Q

What are the signs of tension headache

A

Normal neuro exam

Pericranial/SCM/trapezius/temporalis/lateral pterygoid/masseter tenderness

122
Q

How is tension headache managed?

A

Acute - analgesics

Chronic symptoms (>7-9 headache days/month):
Antidepressants - amitriptyline/doxepin
123
Q

What are the complications of tension headache?

A

Peptic ulcer due to chronic NSAID use

124
Q

What is trigeminal neuralgia?

A

A facial pain syndrome in the distribution of >=1 divisions of the trigeminal nerve

125
Q

Recall the aetiology of trigeminal neuralgia

A

Trigeminal nerve root compression at root entry zone by an aberrant vascular loop (usually superior cerebellar artery)

Demyelinating disease - MS

Other BS lesions

126
Q

What are the risk factors for trigeminal neuralgia?

A

Increased age

MS

127
Q

What are the presenting symptoms of trigeminal neuralgia?

A

Sharp, stabbing, intense pain lasting up to 2m
+ constant facial pain
Without associated neurological deficit

128
Q

What are the signs of trigeminal neuralgia?

A

Normal neuro exam

129
Q

How is trigeminal neuralgia investigated?

A

Clinical diagnosis

Intra-oral XR - ?dental cause
MRI - visualise abnormal vessel loop compressing nerve/tumour/infarct/MS plaque

130
Q

What is Wernicke’s encephalopathy?

A

Neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations, typically involving mental status changes and gait and oculomotor dysfunction

131
Q

What are the risk factors for Wernicke’s encephalopathy?

A 
Alcohol dependence
AIDS
Cancer and chemo
Malnutrition
Hx of GI surgery
132
Q

Recall the aetiology of Wernicke’s encephalopathy

A

Acute or sub-acute thiamine deficiency

As a result of decreased intake, relative deficiency due to increased demand, or malabsorption from GI tract

133
Q

What is the triad in Wernicke’s?

A

Ataxia
Ophthalmoplegia
Confusion

Only 10% present this way

134
Q

How is Wernicke’s encephalopathy investigated?

A
  1. Therapeutic trial of parenteral thiamine - gets better quickly
  2. Finger-prick glucose - normal
  3. Bloods
    Normal = FBC, electrolytes, renal function, ammonia
    Elevated = LFTs, alcohol
    Low = thiamine, Mg
135
Q

What are the presenting symptoms of Wernicke’s encephalopathy?

A

Mental slowing, impaired concentration, and apathy
Frank confusion
Ocular motor findings - gaze palsies, abducens palsies, impaired vestibulo-ocular reflexes

136
Q

What are the causes of raised ICP?

A

Mass effect: brain tumour, infarction w oedema, contusions, SDH, EDH, abscesses - deform adjacent brain

Generalised brain swelling: ischaemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercapnia, Reye hepatocerebral syndrome - decrease cerebral perfusion pressure w minimal tissue shifts

Increased venous pressure: venous sinus thrombosis, HF, obstruction of superior mediastinal/jugular veins

CSF obstruction/overproduction: hydrocephlus, extensive meningeal disease/meningitis, SAH, choroid plexus tumour

Idiopathic intracranial hypertension

Craniosynostosis

137
Q

What are the presenting symptoms of raised ICP?

A 
Headache (morning/wake pt up from sleep/worse on coughing, sneezing, bending/progressively worsening)
Vomiting without nausea
Drowsy/unconscious
Back pain
Visual disturbances
Personality/behavioural changes
138
Q

What are the signs of raised ICP?

A 
Ocular palsies
Altered level of consciousness
Papilloedema
Pupillary dilatation
Cushing's triad - increased SBP, bradycardia, irregular breathing
139
Q

What is myasthenia gravis?

A

a chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction (NMJ) in skeletal muscle

140
Q

What are the risk factors for myasthenia gravis?

A

FHx of AI disorders
Genetic markers - specific HLA genes and single nucleotide polymorphisms in immune system
Cancer-targeted therapy: checkpoint inhibitors

141
Q

What are the presenting symptoms of myasthenia gravis?

A

Muscle fatiguability - worse w activity and improves on rest
Better in morning than evening
Diplopia
Dysphagia
Dysarthria
Proximal limb weakness - difficulty getting out of chair/climbing stairs

142
Q

What are the signs of myasthenia gravis?

A

Ptosis
Facial paresis - flat smile
Proximal limb weakness

143
Q

Recall the aetiology of myasthenia gravis

A

Antibodies against nAChR on post-synaptic muscle membrane at NMJ

Rarely antibodies agaginst muscle-specific tyrosine kinase (MuSK) at NMJ

Certain genotypes (HLA) more susceptible to making these antibodies

144
Q

How is myasthenia gravis investigated?

A
  1. Serum AChR antibody analysis
  2. MuSK antibodies
  3. Serial lung function tests (if SOB) - low FVC and NIF
145
Q

How is raised ICP investigated?

A

?

146
Q

What is neurofibromatosis?

A

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

147
Q

Recall the aetiology of neurofibromatosis

A

Autosomal dominant
Affects cells of neural crest origin
Associated w multiple mutations in TSGs NF1 (type 1) and NF2 (type 2)

148
Q

How many seizures must you have had in order for epilepsy to be diagnosed?

A

2

149
Q

What are the presenting symptoms of neurofibromatosis?

A 
Type 1:
Skin lesions
Learning difficulties
Headaches
Disturbed vision (optic gliomas)
Precocious puberty (pit gland lesions)
Type 2:
Hearing loss
Tinnitus
Balance problems
Headache
Facial pain + numbness
150
Q

What are the signs of neurofibromatosis?

A

Type 1:
5+ café au lait macules of >5mm (pre-pubertal)
5+ café au lait macules of >15mm (post-pubertal)
Neurofibromas - cutaneous nodules or complex plexiform neuromas
Freckling in armpit or groin
Lisch nodules (hamartomas on iris)
Spinal scoliosis

Type 2:
Few or no skin lesions
Sensorineural deafness w facial nerve palsy or cerebellar signs

151
Q

How is neurofibromatosis investigated?

A
  1. MRI/CT/PET - tumours
  2. Biopsy
  3. Genetic testing
  4. Ophthalmological assessment

5 . Audiometry

  1. Skull XR (sphenoid dysplasia in NF1)
152
Q

What is a generalised seizure?

A

Seizure that affects whole of the brain + consciousness

153
Q

What are the 5 types of generalised seizure?

A 
Tonic-clonic
Absence
Myoclonic
Atonic
Tonic
154
Q

Recall the aetiology of epilepsy

A

Most cases are IDIOPATHIC

Primary epilepsy syndromes - eg idiopathic generalised epilepsy

Secondary seizures:
Tumour
Infection
Inflammation
Toxic/metabolic - eg Na imbalance
Drugs - alcohol withdrawal
Vascular - haemorrhage
Congenital abnormalities - cortical dysplasia
Neurodegenerative disease - Alzheimer's
Malignant HTN or eclampsia
Trauma
155
Q

What common things look like seizures?

A

Syncope
Migraine
Non-epileptiform seizure disorder (eg dissociative disorder)

156
Q

What should you ask when taking a history for a potential epilepsy patient?

A 
Rapidity of onset
Duration of episode
Any alteration in consciousness?
Any tongue biting or incontinence?
Any rhythmic sychcronous limb jerking?
Any post-ictal abnormalities eg exhaustion, confusion?
DHx eg alcohol, recreational drugs
157
Q

What are the symptoms of a tonic-clonic seizure?

A

Vague symptoms before attack - irritability
Tonic phase - generalised muscle spasm
Clonic phase - repetitive synchronous jerk
Faecal/urinary incontinence
Tongue biting
Post-ictal phase: impaired consciousness, lethargy, confusion, headache, back pain, stiffness

158
Q

What are the symptoms of an absence seizure?

A

Onset in childhood
Loss of consciousness but maintained posture
Stops talking and stares into space for few seconds
NO post-ictal phase

159
Q

What are the symptoms of a frontal lobe focal motor seizure?

A

Motor convulsions
Jacksonian march - muscular spasm caused by simple partial seizure spreads from affecting distal part of limb towards ipsilateral facce
Post-ictal flaccid weakness (Todd’s paralysis)

160
Q

What are the symptoms of a temporal lobe seizure?

A

Aura - visceral or psychic symptoms

Hallucinations - olfactory or affecting taste

161
Q

What are the symptoms of a frontal lobe complex partial seizure?

A

LOC
Involuntary actions/disinhibition
Rapid recovery

162
Q

Describe non-convulsive status epilepticus

A

Acute confusional state
Often fluctuating
Difficult to distinguish from dementia

163
Q

How is epilepsy investigated?

A

Bloods - FBC, U+E, LFTs, glu, Ca, Mg, ABG, toxicology, prolactin (post-ictal increase)

EEG - helps confirm diagnosis, classify epilepsy

CT/MRI - structural, space-occupying or vascular lesions

164
Q

What are the possible complications of epilepsy?

A
  1. Fractures from tonic-clonic seizures
  2. Behavioural problems
  3. Sudden death in epilepsy (SUDEP)
165
Q

What are the complications of common anti-epileptic drugs?

A

Phenytoin - gingival hypertrophy

Carbamazepine - neutropaenia and osteoporosis

Lamotrigine - Stevens-Johnson syndrome

166
Q

Summarise the prognosis for patients with epilepsy

A

50% remission at 1 year

167
Q

What is status epilepticus?

A

A seizure lasting > 30 mins or repeated seizure without recovery and regain of consciousness in between

168
Q

How is status epilepticus treated?

A

ABC approach

  1. Give glucose if hypoglycaemic
  2. IV lorazepam or IV/PR diazepam
  3. Repeat step 2 after 10 mins if seizure doesn’t stop
  4. If seizure doesn’t stop - IV phenytoin + ECG monitor
  5. If seizure doesn’t stop, GA (thiopentone) + intubation + mech ventilation
  6. TREAT CAUSE
169
Q

How are focal seizures treated?

A

Lamotrigene or carbamazepine

170
Q

How are generalised seizures treated?

A

Sodium valproate

171
Q

List some anti-convulsants

A 
Lamotrigene
Carbamazepine
Sodium valproate
Phenytoin
Levetiracetam
Clobazam
Topiramate
Gabapentin
Vigabatrin
172
Q

What is spinal cord compression?

A

Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury

173
Q

Recall the aetiology of spinal cord compression

A

MOST CASES: trauma and tumours (mets)

Other:
Spinal abscess
TB (Pott’s disease)

174
Q

How can trauma lead to spinal cord compression?

A
  1. Direct cord contusion
  2. Compression by bone fragments
  3. Haematoma
  4. Acute disk prolapse
175
Q

What are the risk factors for spinal cord compression?

A

Trauma
Osteoporosis
Metabolic bone disease
Vertebral disc disease

176
Q

What are the presenting symptoms of spinal cord compression?

A 
Hx of trauma or malignancy
Pain
Weakness
Sensory loss
Disturbance of bowel and bladder function
177
Q

What are the signs of spinal cord compression?

A 
Diaphragmatic breathing
Reduced anal tone
Hyporeflexia
Priapism (persistent and painful erection)
Spinal shock (low BP wo tachycardia)
Sensory loss - at level of lesion
Motor:
- weakness/paralysis
- downwards plantars in acute phase
- UMN signs below lesion
- LMN at level of lesion
178
Q

What can a large central lumbar disc prolapse cause?

A
  1. Bilateral sciatica
  2. Saddle anaesthesia
  3. Urinary retention
179
Q

Identify appropriate investigations for spinal cord compression

A

Radiology:

  1. Lateral radiographs of spine - look for loss of alignment, fractures, etc
  2. MRI/CT

Bloods:
FBC, U+E, Ca, ESR, Ig electrophoresis (multiple myeloma)

Urine:
Bence-Jones proteins (multiple myeloma)

180
Q

What is stroke?

A

Rapid permanent neurological deficit from cerebrovascular insult

Clinically:
Focal or global impairment of CNS function developing rapidly and lasting > 24 hours

181
Q

Recall the aetiology of stroke

A

Infarction (80%):

  1. Thrombosis - lacunar infarcts, in MCA
  2. Emboli - carotid dissection, carotid atherosclerosis, AF
  3. Hypotension
  4. Others - vasculitis, cocaine (arterial spasm)

Haemorrhage (10%):

  1. HTN
  2. Charcot-Bouchard microaneurysm rupture
  3. Amyloid angiopahty
  4. Arteriovenous malformations
    - Less common: trauma, tumours, vasculitis
182
Q

What is a lacunar infarct?

A

Thrombosis in small vessels

183
Q

How can hypotension cause stroke?

A

If the BP is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories

Most distal capillaries vasoconstrict

184
Q

What are the presenting symptoms of stroke?

A 
Weakness
Sensory, visual or cognitive impairment
Impaired coordination
Impaired consciousness
Head or neck pain (if carotid/vertebral artery dissection)
185
Q

What should you ask about in the history for ?stroke?

A

Time of onset (critical for emergency Mx)

Hx of AF, MI, valvular HD, carotid artery stenosis, recent neck trauma or pain

186
Q

What are the signs of a lacunar infarct?

A

Affecting the internal capsule or pons: pure sensory or motor deficit or both

Affecting thalamus: LOC, hemisensory deficit

Affecting basal ganglia: hemichorea, hemiballismus, parkinsonism

187
Q

What are the signs of an anterior cerebral infarct?

A

Lower limb weakness

Confusion

188
Q

What are the signs of a middle cerebral infarct?

A

Facial weakness
Hemiparesis (motor cortex)
Hemisensory loss (sensory cortex)
Apraxia
Hemineglect (parietal lobe)
Receptive/expressive dysphasia (Wernicke’s/Broca’s areas)
Quadrantopia (superior/inferior optic radiations)

189
Q

What is the sign of a posterior cerebral infarct?

A

Hemianopia

190
Q

What are the signs of an anterior inferior cerebellar infarct?

A

Vertigo
Ipsilateral ataxia
Ipsilateral deafness
Ipsilateral facial weakness

191
Q

What are the signs of a posterior inferior cerebellar infarct?

A 
Vertigo
Ipsilateral ataxia
Ipsilateral Horner's syndrome
Ipsilateral hemisensory loss
Dysarthria
Contralateral spinothalamic sensory loss
192
Q

What are the signs of a basilar artery infarct?

A

CN pathology

Impaired consciousness

193
Q

What are the signs of multiple lacunar infarcts?

A 
Vascular dementia
UI
Gait apraxia
Shuffling gait
Normal or excessive arm-swing
194
Q

What are the signs of an intracerebral infarct?

A 
Headache
Meningism
Focal neurological signs
N+V
Signs of raised ICP
Seizures
195
Q

How is stroke investigated?

A

Bloods: clotting profile - check if thrombophilia

ECG - check for arrhythmias

Echocardiogram - identify cardiac thrombus, endocarditis, etc

Carotid doppler US

CT head - rapid detection of haemorrhages

MRI brain - look for infarction

CT cerebral angiogram - dissections or intracranial stenosis

196
Q

How is stroke managed acutely?

A

If < 4.5h from onset:

  1. Exclude haemorrhage by CT head
  2. Thrombolysis - IV ALTEPLASE (tPA)
  3. 300mg ASPIRIN 24h later
  4. Swallowing assessment
  5. Heparin + early mobilisation if high risk of emboli recurrence/stroke progression

If > 4.5h from onset:

  1. Exclude haemorrhage on CT head
  2. ASPIRIN + CLOPIDOGREL
  3. HEPARIN + early mobilisation if high risk of emboli recurrence/stroke progression
197
Q

How is stroke prevented?

A

Aspirin + dipyidamole
Warfarin (AF)
Control RFs: HTN, hyperlipidaemia, treat carotid artery disease
Surgical Tx: carotid endarterectomy

198
Q

What are the possible complications of stroke?

A 
Cerebral oedema - raised ICP
Immobility
Infections
DVT
CV events
Death
199
Q

Summarise the prognosis for patients with stroke

A

10% mortality in 1st month
Up to 50% that survive are dependent on others
10% recurrence within 1 year
Prognosis worse for haemorrhagic than ischaemic

200
Q

What are the different types of neurofibromatosis?

A 
Type 1:
Peripheral + spinal neurofibromas
Multiple café au lait spots
Freckling (armpit/groin)
Optic nerve glioma
Lisch nodules
Skeletal deformities
Phaeochromocytomas
Renal artery stenosis
Type 2:
Schwannomas
Meningiomas
Gliomas
Cataracts
201
Q

What is Parkinson’s disease

A

Neurodegenerative disease of the dopaminergic neurones of the substantia nigra

202
Q

Recall the aetiology of Parkinson’s disease

A

Sporadic/idiopathic:
Most common
Aetiology unknown
May be related to environmental toxins and oxidative stress

Secondary:
Neuroleptic therapy (eg for schizophrenia)
Vascular insults (eg in basal ganglia)
MPTP toxin from illicit drug contamination
Post-encephalitis
Repeated head injury

Some familial forms of PD

203
Q

What are the presenting symptoms of Parkinson’s disease?

A 
Insidious onset
Resting tremor (hands)
Stiffness and slowness of mvmts
Difficulty initiating mvmts
Frequent falls
Smaller handwriting (micrographia)
Insomnia
Mental slowness
204
Q

What are the signs of Parkinson’s disease?

A

Asymmetrical pill-rolling resting tremor - reduced on action

Lead pipe rigidity
- superimposed tremor –> cogwheel rigidity

Stooped, shuffling, small-stepped gait

  • reduced arm swing
  • difficulty initiating walking

Postural instability - falls easily

Frontalis overactivation - furrowed brow
Hypomimic face
Soft monotonous voice
Impaired olfaction
Drooling
Mild impairment of up-gaze
Depression
Cognitive problems and dementia
205
Q

How is Parkinson’s disease investigated?

A

Clinical diagnosis

  1. Levodopa trial - timed walking and clinical assessment after drug
  2. Bloods - serum caeruloplasmin - rule out Wilson’s disease (excess copper) as cause
  3. CT/MRI brain - exclude other causes of gait decline eg hydrocephalus
  4. Dopamine transporter scintigraphy - reduction in striatum and putamen
206
Q

What is a TIA?

A

Transient ischaemic attack

Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours

207
Q

Recall the aetiology of TIA

A

Usually embolic, but may be thrombotic

Most common source of emboli = carotid atherosclerosis

Emboli can also arise from heart: AF, mitral valve disease, atrial myxoma

208
Q

What are the risk factors for TIA?

A 
HTN
Smoking
DM
Heart disease
Peripheral arterial disease
Polycythaemia rubra vera
COCP
Hyperlipidaemia
Alcohol
Clotting disorders
209
Q

What are the presenting symptoms of TIA affecting the 2 most common territories?

A

Usually last 10-15 mins

Carotid:
Unilateral
Motor area: weakness of an arm, leg, or one side of face
Dysarthria
Broac's dysphasia
Amaurosis fugax

Vertebrobasilar:
Homonymous hemianopia
Bilateral visual impairment
Hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia, ataxia

210
Q

What are the signs of TIA?

A

Neuro exam may be normal bc TIA may have resolved
Check pulse for irregular rhythm - AF
Carotid bruits

211
Q

How is TIA investigated?

A

Bloods: FBC, U+E, lipids, LFTs, TSH

Urinanalysis - glycosuria

ECG - AF or previous MI

Unenhanced CT - if possibility of haemorrhage

Investigate for source of emboli - ECG/doppler US of carotid and vertebral arteries

212
Q

How is TIA managed?

A

Acute neuro symps resolved completely within 24h - 300mg aspirin immediately

Assessed urgently within 24h

Confirmed TIA:
Clopidogrel - 300mg loading dose + 75mg thereafter
High-intensity statin therapy - atorvastatin 20-80mg

Secondary prevention:
Antiplatelets
AntiHTNs
Lipid-modifying Tx
AF Mx
213
Q

How do you assess future stroke risk in TIA patients?

A

ABCD2 score

214
Q

What are the possible complications of TIA?

A

Recurrence

Stroke

215
Q

Summarise the prognosis for TIA patients?

A

Very high risk of stroke in first month after TIA and up to a year afterwards

Y3 (20 decks)

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