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CP1 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a good surgical sieve for neurological lesions?

A

VINDIE

Vascular
Inflammation
Neoplastic
Degenerative
Infective
Episodic
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2
Q

Neurology symptoms - sudden tempo causes

A

= vascular/trauma/epilepsy/migraine

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3
Q

Neurology symptoms - hours/days tempo causes

A

= inflammation/infection

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4
Q

Neurology symptoms - days/weeks tempo causes

A

= inflammation/rapid mass lesions

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5
Q

Neurology symptoms - months tempo causes

A

= slower mass lesions

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6
Q

Neurology symptoms - years tempo causes

A

= degenerative

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7
Q

Neurology symptoms - since early life

A

= congenital (can evolve as child grows)

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8
Q

Headache history

A 
Age
Location of Pain
Pattern of pain
Tempo – important for diagnosing cause!
Associated Symptoms
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9
Q

What can cause blackouts/LOC?

what is important to establish from the Hx?

A

epileptic seizures,
fainting attacks,
psychological causes (dissociation),
cardiac causes.

What were they doing before, during, and after?

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10
Q

What is the spinothalamic tract for?

Where do its fibres cross?

A

sensation of pain and temperature.

Crosses near where it enters the spinal cord

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11
Q

UMN and LMN origins

A

UMNs start in the primary motor cortex, within the cerebral hemispheres.

In the medulla this decussates to the other side of the spinal cord (=> corticospinal tract).

This synapses on the anterior horn cell of the spinal cord to a LMN

The LMN synapses on the muscle.

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12
Q

Signs and Symptoms in UMN lesions

A

secondary changes in excitability

Hypertonia, Hyperreflexia, Babinski +ve (extensor plantar), Clonus, weakness

UMN signs can take days to weeks to develop – Pt can be HYPOreflexic in this time.

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13
Q

Signs and Symptoms in LMN lesions

A

shows effects of loss of nerve input to muscle

Hypotonia, Hyporeflexia, Wasting, Fasciculations, weakness

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14
Q

Where is weakness worse in UMN lesions?

A

Extensors of the arm – shoulder abduction, triceps, wrist and finger extensors.

Flexors of the leg – hip flexion, knee flexion, ankle dorsiflexion

(flexors of the arm and extensors of the leg may become stronger to compensate)

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15
Q

What signs and symptoms would you expect with a lesion in the cerebral hemisphere?

A

Contralateral Hemiplegia – arm and leg

Contralateral Motor and sensory signs

UMN signs

May have cognitive signs depending on where the lesion is.
=> Aphasia (L)
=> Spatial neglect (R).

Weakness will SPARE the forehead.

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16
Q

What signs and symptoms would you expect with a lesion in the brainstem?

A

Abnormal eye movements

Vertigo

UMN contralateral or bilateral weakness

Cranial nerve signs and symptoms

+/- Crossed sensory signs

+/- Weakness of face, swallowing and speech

+/- Cerebellar signs

+/- Horners’ sign

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17
Q

symptoms of cerebellar ataxia?

A

impaired coordination in the torso or arms and legs.
frequent stumbling.
an unsteady gait.
uncontrolled or repetitive eye movements.
trouble eating and performing other fine motor tasks.
slurred speech/vocal changes.

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18
Q

What is Horner’s Sign?

Why does it occur?

A

Constricted pupil (miosis),
Drooping of the upper eyelid (ptosis),
Absence of sweating of the face (anhidrosis),
“Sinking” of the eyeball (enophthalmos).

Occurs when there is damage to the sympathetic trunk

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19
Q

What signs and symptoms would you expect with a lesion in the spinal cord?

A

There will be UMN weakness unless the lesion is at the cauda equina.

Typically bilateral weakness, motor and sensory loss.
=> Lesion in thoracic spinal cord – affects legs
=>Lesion in cervical spinal cord – affects arms and legs.

Sensory loss will lead to a “sensory level” above which there is feeling, and below which there isn’t.

Joint position sense, light touch and pain/temp may be differently affected

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20
Q

Where do light touch and joint position sense travel in the spinal cord?

A

dorsal columns

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21
Q

Where do Pain and temperature sense travel in the spinal cord?

A

spinothalamic columns

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22
Q

where does the spinal cord end?

what would a lesion below this additionally effect?

A

L1

typically affect the sphincters, function can be permanently lost.

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23
Q

What signs and symptoms would you expect with a lesion in the root nerve?

A

LMN weakness
Sensory loss
Relevant reflex lost

The pattern of affected muscles and sensory loss is crucial – root or individual nerve distribution?

Anterior horn cell disease (motor neurone disease) will not have sensory loss and may have mixed UMN and LMN signs.

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24
Q

What signs and symptoms would you expect in muscle disease?

A

Proximal weakness is a common pattern – shoulder/thigh muscles.

Neck and respiratory weakness

Eye muscle or swallowing weakness

Muscle that fatigues (weaker with repetitive movement) seen in myasthenia gravis.

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25
Q

What components do you examine in a PNS exam of the limbs?

A 
Inspection
Tone
Power
Reflexes
Coordination and function
Sensation
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26
Q

What visual defect would an ipsilateral optic nerve lesion cause?

A

monocular loss of vision

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27
Q

What visual defect would an optic chiasm lesion lesion cause?

A

bitemporal hemianopia

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28
Q

What visual defect would a contralateral optic tract lesion cause?

A

Homonymous hemianopia

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29
Q

What visual defect would a contralateral optic radiation lesion cause?

A

Homonymous quadrantanopia

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30
Q

What visual defect would a visual cortex lesion cause?

A

Macular sparing in homonymous hemianopia (or quadrantanopia)

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31
Q

What might a trigeminal nerve lesion cause?

A

Wonky/weak jaw

Wasted muscles of jaw

Numb face

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32
Q

Clinical presentation of SAH

A

“Thunderclap” headache
=> develops over seconds, extremely intense, often occipital

Vomiting (after headache begins)
Photophobia
Increasing drowsiness/coma
Focal signs

Neck stiffness
Positive Kernig’s sign – takes 6 hours to develop
Papilloedema – may be present, along with retinal haemorrhages

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33
Q

Why can there be photophobia in SAH?

A

blood can irritate the meninges, causing signs of meningism

aseptic meningitis

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34
Q

Kernig’s Sign

A

Flexion of thighs at the hip, and the knees at 90 degree angles

Assess whether subsequent extension of the knee is painful (leading to resistance)

Resistance leads to positive Kernig’s Sign

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35
Q

When and how can SAH present atypically?

A

particularly in the elderly,

with seizures, confusion or mild headache

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36
Q

What are the causes of SAH?

A
  1. Trauma
  2. Spontaneous:
    - Berry aneurysm
    - Arterio-venous malformation
    - Cryptogenic
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37
Q

Which conditions/factors which can predispose someone to SAH?

A

Marfan’s and Ehler’s Danlos Syndrome
Polycystic kidney disease
Smoking and ETOH

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38
Q

Where do Berry Aneurysms most commonly develop?

A

Anterior communicating artery – most common

Posterior communicating artery

Middle cerebral artery

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39
Q

risk factors for berry aneurysm

A

More common in PCKD

FHx, smoking, HTN, connective tissue disorders

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40
Q

AV Malformation

A

Congenital collection of abnormal arteries/veins

Have a tendency to re-bleed if symptomatic once

A cause of SAH and also sometimes epilepsy

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41
Q

Complications of SAH

A

Death (30% die immediately)

Rebleed (3-4 days for aneurysm, years for AVM)

Hydrocephalus - fibrosis in CSF pathways

Cerebral vasospasm

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42
Q

Subdural haematoma

A

= a collection of blood in the subdural space following the rupture of a vein.

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43
Q

Acute SDH Presentation

A

Within 72 hours.

Occurs in severe acceleration-deceleration head injury, often with co-existing brain damage.

LOC, low GCS, anisocoria, motor deficit

May be a lucid interval

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44
Q

What is a Lucid interval in SDH?

A

The patient can appear relatively well and normal for a few hours after the injury, but subsequently deteriorates and LoC as the haematoma forms

45
Q

How will acute SDH appear on CT?

A

appear hyperdense on CT – classic cresenteric shape of white density

46
Q

Sub-acute SDH Presentation

A

May occur spontaneously, or after minor trauma

Signs and symptoms of raised ICP being to develop ~2 weeks after the insult or start of the bleed, and are often more subtle/fluctuant

47
Q

what are risk factors for sub-acute SDH?

A

The elderly – cerebral atrophy and increased venous fragility

Alcohol abuse – clotting is reduced

Seizures

Anti-coagulants and coagulopathies

48
Q

How can sub-acute SDH appear on CT?

A

blood may be isodense or hypodense to the brain parenchyma

49
Q

What are some signs of raised ICP?

A 
Headache
Drowsiness
Confusion
Focal neurological signs
Eventually stupor and coma occur.
50
Q

Complications of SDH

A

Death
Raised ICP
Cerebral oedema.

Recurrent haematoma formation during recovery.

Seizures.

Wound infection, subdural empyema, meningitis.

Permanent neurological or cognitive deficit due to pressure effects on the brain.

Coma/persistent vegetative state.

51
Q

What is a stroke?

A

= an acute, focal neurological deficit of cerebrovascular origin that persists >24 hours

52
Q

What is a TIA?

A

= an acute, focal neurological deficit of cerebrovascular origin that persists <1 hour, without signs of cerebral infarction on MRI scanning.

very high risk of stroke within 4 weeks of TIA

53
Q

What is Amaurosis Faugax ?

A

= sudden, transient loss of vision in one eye.

occurs in TIA of the retina
Can also occur due to ocular disease or migraine

54
Q

What are the types of stroke?

A
  1. ~85% ischaemic

2. ~15% haemorrhagic.

55
Q

Causes of ischaemic stroke

A

Arterial embolus from a distant site

Arterial thrombosis in atheromatous carotid/vertebral/basilar artery

Systemic hypoperfusion (general circulatory problem)

56
Q

Causes of haemorrhagic stroke

A

Sub-arachnoid haemorrhage

Intra-cerebral haemorrhage

57
Q

Risk factors for Ischaemic Stroke

A 
NON-MODIFIABLE
Age
Male sex
Family History
Hypercoagulable states
Non-white ethnicity
AF
MODIFIABLE:
Hypertension
Hypercholesterolaemia
Diabetes
Smoking
Alcohol 
Poor diet
Low exercise
Increased weight
Use of oestrogen-containing oral contraceptives
58
Q

Risk factors for Haemorrhagic Stroke

A

Family History
Uncontrolled HTN
Vascular abnormalities (aneurysms, AVMs, HHT)
Coagulopathies/anticoagulant therapies
Heavy recent alcohol intake.
Illicit drug use (mostly amphetamines and cocaine)
Trauma

59
Q

What are the clinical features of a stroke?

A

typical of hemispheric lesion:

Facial weakness – sparing forehead.

Contralateral limb weakness/hemiplegia and loss of sensation.

Higher Dysfunction

60
Q

What are forms of Higher Dysfunction?

A

Expressive aphasia

Receptive aphasia

Apraxia

Asterognosis

Agnosis

Inattention (neglect)

61
Q

Apraxia

A

difficulty in performing task, despite intact motor function.

62
Q

Asterognosis

A

inability to identify objects in both hands, despite intact sensation.

63
Q

Agnosis

A

inability to recognise objects/people/sounds/smells despite the specific sense intact and no memory loss.

64
Q

Inattention (neglect)

A

inability to attend to stimuli despite intact senses.

65
Q

Expressive aphasia

A

inability to express language despite intact comprehension

66
Q

Receptive aphasia

A

inability to understand commands, may have fluent but meaningless speech

67
Q

What investigation is required for suspected stroke?

A

urgent CT - identify if ischaemic or haemorrhagic

68
Q

Total Anterior Circulation Syndrome (TACS)

A

= proximal MCA occlusion

Affecting the areas of the brain supplied by both the middle and anterior cerebral arteries

All three of:

  1. Higher dysfunction (incl. decreased level of consciousness)
  2. Homonymous hemianopia
  3. Contralateral hemiplegia and/or sensory loss (>2 of face, arm, leg)
69
Q

Partial Anterior Circulation Syndrome (PACS)

A

= distal MCA or ACA occlusion
A less severe form of TACS, in which only part of the anterior circulation has been compromised.

Requires 2 of the 3 TACS criteria.

70
Q

Lacunar Stroke (LACS)

A

= occlusion of lacunar branch of MCA

A subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions.

One of the following:

  • Pure motor symptoms
  • Pure sensory symptoms
  • Pure sensorimotor symptoms
  • Ataxic hemiparesis
71
Q

Posterior Circulation Stroke (POCS)

A

= PCA occlusion.

There will be damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum, thalamus, and brainstem).

Presents as:

  • Cranial nerve palsy AND contralateral motor/sensory deficit.
  • Conjugate eye movement problems (e.g. nystagmus, double vision)
  • Cerebellar dysfunction
  • Isolated homonymous hemianopia
72
Q

What are complications of a stroke?

A

Cognitive impairment

MI, Heart failure

Dysphagia

Aspiration pneumonia

UTI

DVT, PE

Dehydration, malnutrition

Pressure sores

Depression

Orthopaedic complications and contractures

73
Q

What is the association of AF with stroke?

A

The left atrial appendage is the usual site of thrombus formation in AF.

Stasis of blood leads to formation of a thrombus.

Thrombus can embolise to the posterior/anterior cerebral circulation, causing embolic stroke.

74
Q

what is meningism?

A

= meningeal irritation

75
Q

Symptoms and signs of meningism

A
  • Global headache
  • Neck and back stiffness
  • Nausea and vomiting
  • Photophobia

Signs:

  • Nuchal rigidity – neck resists flexion.
  • Brudzinski sign – flexion of the neck results in hip flexion
  • Kernig’s sign – knee extension elicits pain and resistance to further extension.
76
Q

what is Brudzinski’s sign?

A

positive when flexion of the neck results in hip flexion

77
Q

what is Kernig’s sign?

A

positive when knee extension elicits pain and resistance to further extension

78
Q

what is meningitis?

A

= inflammation of the meninges.

79
Q

What are the routes of infection to the meninges?

A
  • Blood-borne
  • Para-meningeal suppuration - e.g. otitis media, sinusitis
  • Direct spread through a defect in the dura - e.g. post-surgery, trauma
  • Direct spread through the cribriform plate (rare)
80
Q

What is a sign of a defect in the dura?

A

CSF leaking out of the nose/ear is a sign of a defect in the dura

81
Q

Complications of meningitis

A
  • Death
  • Subdural collection of pus
  • Cerebral vein thrombosis
  • Hydrocephalus

• 9-15% deafness - particularly in children, associated with Hib infection

  • Convulsions
  • Visual/motor/sensory deficit
82
Q

How can meningitis cause hydrocephalus?

A

subsequent scarring can alter CSF absorption, accumulation of CSF can cause expansion of ventricles

83
Q

What are the common bacterial causes of meningitis?

What age groups are affected?

A

Neisseria meningitidis - Children, Young adults

Streptococcus pneumoniae - Elderly, Children <2 years

(Haemophilus influenzae type B, Hib) - Children <5 years

Escherichia coli - Neonates

Listeria monocytogenes - Neonates, Immunocompromised

Streptococcus agalactiae (Group B Strep) -Neonates

84
Q

What are the viral causes of meningitis?

A

Enterovirus, HSV, VZV, EBV, Mumps.

85
Q

Clinical features of meningitis

A

Classic clinical triad = headache, fever and neck stiffness

  • Global headache
  • Neck and back stiffness
  • Nausea and vomiting
  • Photophobia

Others:

  • Seizures
  • Focal neurological symptoms
  • Lethargy and confusion
  • Stupor and Coma
86
Q

when can meningitis present atypically?

A

may be observed in the very young, very old or immunocompromised

87
Q

Neurological signs of meningitis

A
  • Impaired conscious level
  • Cranial nerve palsies – due to RICP or direct damage (principally 3,4,6 or 7)
  • Focal or generalised seizures
  • Papilloedema and other signs of RICP
  • Focal neurological signs – e.g. hemiparesis, dysphasia, hemianopia due to ischaemia from vascular inflammation (arteritis or venous thrombophlebitis)
  • Sensorineural deafness
88
Q

Systemic signs of meningitis

A
  • Pyrexia
  • Extracranial infection (e.g. sinusitis, otitis media, mastoiditis, pneumonia)
  • Arthritis (N. meningitidis)
  • Endocarditis
  • Skin – Non-blanching petechial/purpuric rash (suggesting meningocococcaemia)
  • Endotoxic shock
89
Q

Investigation of meningitis - bedside tests

A

FBC, U&E, LFT, CRP, Clotting, Blood cultures
Meningococcal/pneumococcal PCR
Lactate, Glucose
Throat swab

?Stool sample
?HIV

90
Q

Investigation of meningitis - imaging/invasive

A

CT, MRI (do not delay LP unless signs of raised ICP)

LP (if possible)
=> Opening Pressure
=> CSF – Protein, cell count, MCS, glucose (+serum glucose), vPCR

91
Q

what are signs of raised ICP that may mean a lumbar puncture is contraindicated?

A
  • GCS <12
  • Seizures
  • Focal neurological signs

• Papilloedema (can be slow in its development and lack of papilloedema does not rule out raised ICP)

92
Q

what are some other contraindications for lumbar puncture (other than raised ICP)

A

Signs of meningococcal septicaemia

Evidence of potential bleeding risk (platelets <50, INR >1.2)

History of clotting disorder

93
Q

CSF composition - bacterial meningitis

A

Extremely elevated leucocytes
=> mainly neutrophils

raised protein

low glucose

94
Q

CSF composition - viral meningitis

A

elevated leucocytes
=> mainly lymphocytes (unless early presentation)

slightly raised protein

normal glucose

95
Q

CSF composition - TB meningitis

A

elevated leucocytes
=> mainly lymphocytes (unless early presentation)

very raised protein

very low glucose

96
Q

What glucose level in the CSF is normal?

A

60-80% of serum levels.

97
Q

How is meningitis managed?

A
  • Antibiotics
  • Adequate oxygenation
  • Prevention of hypoglycaemia and hyponatraemia
  • Anticonvulsants – if patient is fitting
  • Decrease ICP – prevent brain herniation
98
Q

Viral encephalitis - clinical features

A 
Fever
	Seizures
	Altered mental state
	Headache 
	Focal neurological deficit
99
Q

How is viral encephalitis investigated?

A

in the same way as meningitis

100
Q

How is viral encephalitis managed?

A 
IV aciclovir (oral not acceptable)
Aggressive management of seizures

Even if the LP picture does not add up to viral encephalitis, if there is enough clinical suspicion then you should treat with IV acyclovir

101
Q

Cerebral abscess - clinical presentation

A

Presentation will depend on the location of the abscess

  • Focal neurological signs
  • Raised ICP
  • Headache 70-95% (short duration)
  • Fever variable
  • CRP and ESR raised

• (CSF pleocytosis - if done before suspicion of brain abscess – contraindicated to do lumbar puncture if raised ICP is suspected))

102
Q

CNS infections in the immunocompromised

A

More susceptible to less common organisms

They may not respond to usual meningitis treatment

103
Q

Dysdiadochokinesis

A

= the inability to execute rapidly alternating movements, particularly of the limbs

e.g. demonstrated by asking the patient to pronate and supinate an arm at speed

104
Q

What signs can lesions of the cerebellum cause?

A 
Dysdiadochokinesis
Ataxia
Nystagmus
Intension Tremor
Slurred Speech
Hypotonia
105
Q

CT vs MRI in neurology

A

CT is preferred in the acute setting - intracranial haemorrhage and (broadly) tumours and abscesses

MRI superior in detecting most other things.

106
Q

How does a subarachnoid haemorrhage normally present on CT?

A

hyperdensity within the sulci of the brain

107
Q

How does a parenchymal haemorrhage normally present on CT

A

a focal area of hyperdensity, sometimes surrounded by an area of low density, which is parenchyma oedema.

108
Q

what are the two types of cerebral parenchymal oedema?

A
  1. Vasogenic oedema:
    • Normally associated with tumour
    • Involves white matter, spares cortex.
  2. Cytotoxic oedema:
    • Oedema is diffuse and involves both the grey and white matter.
    • Tends to be seen in strokes.

CP1 (12 decks)

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