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CP1 > Neurology > Flashcards

Neurology Flashcards

1
Q

What does the anterior cerebral artery supply?

A

Medial surface of cerebral hemisphere until the peri-occipital sulcus

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2
Q

Where does the middle cerebral artery supply?

A

2/3 of the lateral surface of the brain

Central branches supply the corpus striatum, thalamus and internal capsule

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3
Q

Where does the posterior cerebral artery supply?

A

Corpus callosum
Cortex of occipital and temporal lobes
Central branches supply the optic radiation, subthalamic nucleus and thalamus

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4
Q

Which arteries are the brainstem and cerebellum supplied by?

A

Vertebral and basilar

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5
Q

CN I functions

A

Olfactory

Special sensory: smell from nasal mucosa

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6
Q

CN II functions

A

Optic

Special sensory: vision from retina

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7
Q

CN III functions

A

Oculomotor
Somatic motor: medial, superior, inferior rectus muscles, inferior oblique
Visceral motor: pupil constriction

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8
Q

CN IV functions

A

Trochlear

Somatic motor: superior oblique extra-ocular muscle

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9
Q

CN V functions

A

Trigeminal
Opthalmic V1: sensory superior 1/3 of face + cornea
Maxillary V2: sensory median 1/3 of face
Mandibular V3: sensory mandible + lower lip, motor=masseter & pterygoids/muscles of mastication

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10
Q

CN VI functions

A

Abducent

Somatic motor: lateral rectus extra-ocular

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11
Q

CN VII functions

A

Facial
Somatic motor: muscles of facial expression
Visceral motor: submandibular/sublingual glands, lacrimal glands
Special sensory: taste from anterior 2/3 of tongue
General sensory: skin of external acoustic meatus

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12
Q

CN VIII functions

A

Vestibulocochlear

Special sensory: hearing (vestibular) and balance (cochlear)

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13
Q

CN IX functions

A

Glossopharyngeal
Somatic motor: stylopharyngeus
Visceral motor: parotid gland
Special sensory: posterior 1/3 of tongue
General sensory: external ear and pharynx sensation
Visceral sensory: visceral feedback from carotid body

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14
Q

CN X functions

A

Vagus
Somatic motor: palatal/laryngeal/pharyngeal muscles of swallowing
Visceral motor: parasympathetic innervation to smooth muscles of the trachea, bronchi, digestive tract, heart
Visceral sensory: sensation from trachea, bronchi, digestive tract, heart
Special sensory: taste from epiglottis/palate
General sensory: sensation from auricle and external acoustic meatus

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15
Q

CN XI functions

A

Accessory

Motor: sternocleidomastoid & trapezius

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16
Q

CN XII functions

A

Hypoglossal

Intrinsic/extrinsic muscles of the tongue

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17
Q

CN nuclei

A 
CN I: olfactory epithelium
CN II: retinal ganglion cells
CN III & IV: midbrain
CN V, VI, VII: pons
CN VIII: vestibular/spinal ganglion
CN IX, X, XII: medulla
CN XI: spinal cord
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18
Q

Bulbar palsy clinical presentation

A

LMN weakness of muscles supplied by cranial nerves with cell bodies within the medulla: IX, X, XII
Tounge: wasted, flaccid, fasciculating, fast movements
Dysphagia?
Soft palate elevation?
Quiet, nasal speech?
Jaw jerk/gag reflex absent?

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19
Q

Pseudobulbar palsy clinical presentation

A

Bilateral UMN disease of medullary cranial nerves
Tongue: stiff/spastic, slow movements, no wasting
Dysphagia?
Normal soft palate elevation
Gravelly ‘donald duck’ speech / slurred high pitched dysarthria
Exaggerated jaw jerk
Mood disturbances

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20
Q

Causes of bulbar palsy

A 
Degenerative: motor neurone disease
Vascular: stroke
Inflammatory: Guillain-barre
Infective: botulism
Neoplastic: brainstem tumours
Congenital
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21
Q

Causes of pseudobulbar palsy

A

Degenerative: MND
Vascular: stroke
MS
Head trauma

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22
Q

Frontal cerebral hemisphere lesion presentation

A

Intellectual impairment, personality change
Urinary incontinence
Mono/hemiparesis
Broca’s aphasia (if left frontal)

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23
Q

Left temporo-parietal cerebral hemisphere lesion presentation (dominant hemisphere)

A 
Agraphia: inability to write
Alexia: word blindness
Acalculia: inability to calculate
Wernicke's aphasia
Contralateral sensory neglect
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24
Q

Right temporo-parietal cerebral hemisphere lesion presentation

A

Failure of face recognition

Contralateral sensory neglect

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25
Q

Occipital cerebral hemisphere lesion presentation

A

Visual field defects

Visuospatial defects

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26
Q

Lateral cerebellar lesion presentation

A

Ipsilateral pathological signs
Broad, ataxic gait: test heel-toe walking, +ve Rhomberg test suggests sensory (rather than cerebellar) ataxia
Titubation: rhythmic head tremor
Dysarthria: slurred, staccato speech
Nystagmus: towards the side of the lesion
Dysmetric saccades: inability to change eye focus
Upward drift (if pronator drift also present = UMN pathology also)
Rebound phenomenon
Hypotonia: decreased in pure cerebellar disease
Mild hyporeflexia
Dysmetria: imprecise coordination
Dysdiadochokinesis: clumsy rapid alternating movements

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27
Q

Cerebellar examination investigations

A

Full neurological exam
TFTs
Antineuronal antibodies
MRI brain

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28
Q

Midline cerebellar lesion presentation

A

Rolling, broad, ataxic gait
Difficulty standing/sitting unsupported
Cannot perform Rhomberg’s with eyes open/closed
Vertigo/vomiting if extension into 4th ventricle

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29
Q

Causes of bilateral cerebellar dysfunction

A

Alcohol
Drugs: phenytoin, anti-epileptics
Paraneoplastic cerebellar degeneration: antineuronal antibodies present, common with breast/SCC of lung
Severe hypothyroidism

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30
Q

Causes of unilateral cerebellar dysfunction

A

MS
Stroke
Tumour: acoustic neuroma, meningioma

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31
Q

Components of the basal ganglia

A

Corpus striatum: caudate nucleus, globus pallidum, putamen
Subthalamic nucleus
Substantia nigra
Parts of the thalamus

32
Q

Basal ganglia lesion presentation

A

Bradykinesia progressing to akinesia: slowness of movement/loss of power of voluntary movement
Muscle rigidity
Involuntary movements…
Tremor
Dystonia: spasms
Athetosis: writhing involuntary movements of hands/face/tongue
Chorea: jerky involuntary movements
Hemiballismus: violent involuntary movements, proximal muscles of one arm

33
Q

Clinical syndromes resulting from basal ganglia pathology

A

Parkinsonism
Huntingtons
Hemiballismus

34
Q

Causative lesion of a central scotoma

A

Macula lesion e.g. diabetic maculopathy

35
Q

Causative lesion of monocular loss of vision

A

Ipsilateral optic nerve lesion

36
Q

Causative lesion of bitemporal hemianopia/quadrantopia

A

Optic chiasm lesion
Affects the nasal fibres from each eye
Superior bitemporal quadrantanopia: pressure from below chiasm (e.g. pituitary tumour)
Inferior bitemporal quadrantanopia: pressure from above the chiasm (craniopharyngoma, carotid aneurysm, meningioma)

37
Q

Causative lesion of homonymous hemianopia

A

Contralateral optic tract lesion

38
Q

Causative lesion of homonymous quadrantanopia

A

Contralateral optic radiation lesion…
Temporal lesion: superior homonymous quadrantopias
Parietal lesion: inferior homonymous quadrantopias

PITS = parietal inferior, temporal superior

39
Q

Causative lesion of macular sparing homonymous hemianopia/quadrantanopia

A

Defect in visual cortex (occipital lobe)

40
Q

LMN signs

A 
LMN innervate ipsilateral muscles
Weakness
Wasting
Fasciculations
Hypotonia
Hyporeflexia
Ipsilateral facial weakness in muscles of facial expression
41
Q

LMN lesion differentials

A

Ventral horn pathology: MND, post-polio
Peripheral nerve pathology
Neuromuscular junction pathology: myasthenia gravis
Muscular pathology

42
Q

UMN signs

A 
UMN innervate contralateral muscles
Weakness: upper limb extensors, lower limb flexors
No wasting
Hypertonia, spasticity
Hyperreflexia
Loss of fine motor movements
Pronator drift
Extensor plantar response: Babinski
Clonus
Contralateral face weakness (sparing frontalis): brow furrowing, eye closing and blinking are preserved
43
Q

UMN lesion differentials

A 
Vascular: stroke
Inflammatory: MS, MND
Neoplastic: tumour
Degenerative: Parkinson's
Infective: post-meningitis
Drugs
44
Q

Spinothalamic tract anatomy

A

Trasmits pain, temperature, light touch to the thalamus

Decussates at spinal level

45
Q

Dorsal columns anatomy

A

Fasciculus cuneatus & gracilis
Transmits deep touch, propriception & vibration to pariatel cortex
Decussates at brainstem

46
Q

Corticospinal tracts anatomy

A

Transmits motor axons from the motor cerebral cortex to the spinal cord
Decussates at the brainstem

47
Q

Stroke definition

A

Acute, focal, neurological deficit of cerebrovascular origin that persists >24h

48
Q

Transient ischaemic attack definition

A

Acute, focal neurological deficit of cerebrovascular origin that persists <1h
MRI: no signs of cerebral infarction
High risk of stroke within 4w of a TIA

49
Q

Amaurosis fugax definition

A

Sudden transient loss of vision in one eye
Often occurs with TIAs
Can be 1st clinical sign of inferior cerebral artery stenosis
Can occur due to ocular disease, migraine

50
Q

Irreversible risk factors for ischaemic stroke

A

Age
Personal/family history
Hyper-coagulable states
AF

51
Q

Reversible risk factors for ischaemic stroke

A 
Hypertension
Hypercholesterolaemia
DM
Smoking
Alcohol
Poor diet
Low exercise
Increased weight
Endocarditis
Migraine
Polycythaemia
APL syndrome
Vasculitis
Amyloidosis
52
Q

Risk factors for haemorrhagic stroke

A 
Family history
Uncontrolled hypertension
Vascular abnormalities: aneurysms, atriovenous malformation, hereditary haemorrhagic telangiectasia
Coagulopathies/anticoagulant therapy
Recent heavy alcohol intake
53
Q

Types of cerebral ischaemia

A

Regional infarction: thrombosis/embolus in large vessels, usually cortical areas

Lacunar infarction: microinfarcts caused by arteriosclerosis, ususally sub-cortical, can be asymptomatic –> pseudoparkinsonism/vascular dementia

Global ischaemia: infarcts at arterial boundary zones due to severe hypotension (watershed infarct)
Severe: cortical laminar necrosis in 24h = vegetative state

54
Q

Zones of cerebral ischaemic damage

A

Infarct core: tissue almost certain to die
Oligaemic periphery: tissue that will survive due to collateral supply
Ischaemic pneumbra: tissue in between

55
Q

Clinical features of ischaemic stroke

A 
Contralateral limb weakness/hemiplegia: first flaccid, then hyperreflexia, weakness recovers gradually over weeks/months
Facial weakness
Higher dysfunction
Visual disturbances
Epileptic fit (rare)
56
Q

Higher dysfunction in ischaemic stroke

A

Expressive aphasia: Broca’s
Receptive aphasia: Wernicke’s
Apraxia: difficulty performing tasks despite intact motor function
Asterognosis: inability to recognise objects, persons, sounds, shapes or smells despite senses/memory being intact
Inattention: inability to attend to stimuli despite intact senses

57
Q

Subarachnoid haemorrhage clinical presentation

A

‘Thunderclap headache’: comes on in seconds, high intensity, often occipital, during transient hypertension
Vomiting: post-headache
Photophobia
Increasing drowsiness/coma
Focal signs: may help locate lesion, may reflect raised ICP / cerebral vasospasm
Neck stiffness
Kernig’s sign +ve
Papilloedema: + retinal haemorrhages
Prior ‘sentinel headache’: small warning leak from offending aneurysm

58
Q

Subarachnoid haemorrhage predisposing abnormalities

A 
Berry aneurysm (70%)
Arteriovenous malformations (AVM - 10%)
No lesion found (20%)
59
Q

Berry aneurysm locations

A

Developmental (not congenital)
In circle of Willis and adjacent arteries…
Anterior communicating artery (most common)
Posterior communicating artery: at bifurcation from inferior cerebral artery
Middle cerebral artery: at bi/trifurcation

60
Q

Berry aneurysm risk factors

A 
Polycystic kidney disease
Family history
Smoking
Hypertension
Ehlers-Danlos/Marfans
61
Q

Arteriovenous malformation pathology

A

Congenital collection of abnormal arteries/veins
10% rebleed annually
Can cause focal epilepsy

62
Q

Subarachnoid haemorrhage complications

A

Death: 30%
Re-bleed: vasospasm clot from aneurysm holds for 3-4 days, AVMs rebleed within a few years
Hydrocephalus: fibrosis in the CSF pathway
Cerebral vasospasm: severe - delayed ischaemic damage

63
Q

Acute subdural haematoma cause & presentation

A

Severe acceleration-deceleration head injury with co-existing brain damage
Young
Dilated pupil
No lucid interval before decreased GCS

64
Q

Subacute/spontaneous subdural haematoma risk factors

A

Spontaneous/minor trauma

Elderly: cortical atrophy stretches brittle veins
Alcohol abuse: clotting is reduced
Coagulopathies

65
Q

Subacute/spontaneous subdural haematoma presentation

A 
Symptoms/signs of raised ICP develop around 3w after start of bleed, often fluctuant
Headache
Drowsiness
Confusion
Focal neurological signs
Eventually: stupor &amp; coma
66
Q

CT presentation of acute subdural haematoma

A

Classical crescenteric shape with increased density (white)
Conforms to contour of the skull
May be accompanying midline shift & compression of ventricles

67
Q

CT presentation of chronic subdural haematoma

A

Blood becomes more radiolucent (dark)

Assumes lentiform shape similar to an extradural haematoma

68
Q

Causes of bacterial meningitis

A

Neisseria meningitidis: classic petechial rash, occurs in small epidemics
Streptococcus pneumoniae: more common if skull fractures, ear disease, congenital CNS lesions

Remainder (30%): Listeria monocytogenes (elderly/immunosuppressed), Haemophilus influenzae, Staph. aureus, TB

69
Q

Viral causes of meningitis

A

Enteroviruses: coxsakievirus A/B, echoviruses
HSV
VZV

70
Q

Clinical presentation of bacterial meningitis

A 
Meningitic syndrome: headache, neck stiffness, fever
High fever + rigors
Photophobia
Malaise
Vomiting
Confusion &amp; seizures
Kernig's sign +ve
Brudzinski sign +ve
Signs of raised ICP / cranial nerve palsies
71
Q

Meningitis complications

A

Venous sinus thrombosis
Severe cerebral oedema
Hydrocephalus

72
Q

Meningococcal meningitis presentation & causes

A

Petechial rash: erythematous, non-blanching purpura
Carried in nasopharynx
Most caused by meningitis C/B
Meningitis ACWY jab at 14y

73
Q

Viral meningitis presentation

A

Almost always a benign, self-limiting condition
4-10d
Headache following for months

74
Q

TB meningitis presentation

A

Insidious illness with fever, weight loss, progressive confusion/cerebral irritation –> coma
May present as per bacterial meningitis

75
Q

Meningitis investigations

A

Bloods: FBC, U&Es, LFTs, clotting, glucose, lactate
Serum PCR: pneumococcal & meningococcal antigens
Blood cultures: prior to abx
Lumbar puncture: if clinical suspicion of a mass lesion: send for MCS protein, glucose, PCR
CT prior to lumbar puncture: if suspected raised ICP
2x throat swabs: virology + bacteriology

76
Q

CSF stains demonstrating organisms

A

Gram +ve intracellular diplococci: Pneumococcus
Gram -ve cocci: Meningococcus
Ziehl-Neesen stain for acid-fast bacilli: TB
Indian stain: fungi

77
Q

CSF findings for bacterial/TB/viral meningitis/encephalitis

A

Bacteria: tubid fluid, high polymorphs
Virus: clear fluid, high lymphocytes, normal glucose
TB: raised lymphocytes, raised polymorphs

CP1 (12 decks)

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