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CP1 revision > Deck 11 > Flashcards

Deck 11 Flashcards

1
Q

Acute neuro lesions

A

Could be vascular, episodic or infective

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2
Q

Subacute neuro lesions

A

could be inflammatory, neoplastic or infective

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3
Q

Chronic neuro lesions

A

could be degenerative, neoplastic or infective

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4
Q

movement based neuro lesions

A

consider basal ganglia, cerebellum (ipsilateral) or corticospinal

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5
Q

sensation based neuro lesions

A

could be dorsal column (crosses after nuclei in medulla) or spinothalamic (cord cross)

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6
Q

Cord lesions

A

Generally bilateral unless brown sequard syndrome

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7
Q

Brainstem lesions

A

ipsilateral CN sign, contralateral peripheral nerve sign

Brainstem infarction often has vertigo as finding

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8
Q

nerve root pattern

A

pain at nerve root, then on corresponding dermatome

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9
Q

focal nerve lesion

A 
isolated lesions (although if multiple then mononeuritis multiplex)
Could be diabetes or vasculitis
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10
Q

Peripheral neuropathy

A

Sensory defect, may have weakness. Typically distal, symmetrical, glove and stocking. Typical of diabetes

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11
Q

muscle disease features

A

weakness only, no sensory issues

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12
Q

Myasthaenia gravis

A

arms, legs, eyes and mouth

Progressive weakness over the course of the day. NMJ pathology

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13
Q

Problem at right optic nerve

A

monocular vision loss (R)

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14
Q

optic chiasm lesion

A

Bitemporal heminaopia)

If pituitary tumour, may get superior quadrantanopia

If craniopharyngioma, carotid aneurysm or meningioma then may get inferior quadrantanopia

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15
Q

Right optic tract lesion

A

honomymous hemianopia (left visual field defect)

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16
Q

Problem at right temporal lobe (optic lesion)

A

Meyers loop - superior quadrantanpia of left visual field

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17
Q

Problem at right parietal lobe (optic lesion)

A

causes inferior quadrantic heminaopia of left visual field

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18
Q

Problem at cortex (e.g. right) - optic lesion

A

contralateral (left) homonoymous hemianopia (macula sparing)

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19
Q

CNIII lesion

A

ptosis, mydriasis, down and out eye (unopposed SO)

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20
Q

CNIV lesion

A

nasal upshot, vertical diplopia. Head tilts away from affected side

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21
Q

CNVI lesion

A

abduction issue, slight adduction in forward gaze

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22
Q

CNVII lesion

A

See frontal sparing in UMN lesion, or complete paralysis in Bell’s or ramsay hunt

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23
Q

CNX lesion

A

uvula deviates away from affected side, soft palate fails to rise

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24
Q

CNXII

A

tongue deviates towards affected side

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25
Q

Investigation with sudden neurological deficit

A

Urgent CT

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26
Q

Distinction between stroke and TIA

A

stroke is sudden onset syndrome of neurological distubance lasting 24h plus or leading to death. TIA reverses within 24h.
TIA can include amaurosis fugax lasting 1 min to 1 hour.

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27
Q

amaurosis fugax

A

seen in TIA, papiloedema (seconds), migrane aura (up to 30 mins)

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28
Q

Thalamus blood supply

A

Supplied by posterior cerebral artery - ischaemia causes sensory loss/distubance)

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29
Q

Brainstem blood supply

A

Basilar, superior cerebellar, anterior inferior cerebellar. Ischaemia gives limb weakness, sensory loss, CN palsy, locked in syndrome

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30
Q

Cerebellum blood supply1

A

Superior, anterior inferior and posterior inferior cerebral arteries. Ischaemia causes vertigo, ataxia, nystagmus and cerebellar signs

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31
Q

Occipital lobe blood supply

A

Posterior cerebral artery, ischaemia causes visual field defect

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32
Q

Ischaemic stroke on CT

A

dense artery

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33
Q

Stroke types

A

85% ischaemic (can be thrombotic, embolic, systemic hypoperfusion, vasculitis (systemic inflammation promotes pro-coagulation state). 15% haemorrhagic

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34
Q

Stroke RF

A

HTN, T2DM, hyperlipidaemia, AF, smoking, carotidy artery disease, obesity, metabolic syndrome, age, menopaiuse, male FHx, non white, syphillis

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35
Q

Lacunar infarctions

A

microinfarcts, arteriolosclerosis - often affects basal ganglia.
Can give vascular dementia

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36
Q

global ischaemia

A

Infarcts at boundary zones (watershed infarction) - if severe can give vegetative state (post arrest syndrome)

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37
Q

ischaemia parts (e.g. penumbra)

A

infarct core, oligaemic periphery (needs collateral supply) and ischaemic penumbra in betweeen (variable outcome tissue)

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38
Q

Stroke histology

A

1-2 days: axon hypoxia, myelin unravels, axons swell and degenerate (softening)
1-2 weeks, core disintegrates, neovascularisation and digestion of products
1-2 months -astrocytes proliferate and cause a glial scar around infarct

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39
Q

TACS

A

From internal carotid, affects anterior and middle cerebral arteries.

Causes hemivisual defect (MCA) - honomymous hemianopia), weakness/sensory defecit and higher cortical dysfunction (loc, dysphasia, visuospatial awareness)

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40
Q

PACs

A

As per TACS , but only 2 of
○ Hemivisual defect from optic radiation dysfunction via MCA (homonomyous hemipanopia)
○ Weakness/sensory deficit
Higher cortical dysfunction (LoC, dysphasia, visuospatial awareness)

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41
Q

POCS

A

1 of:
○ CN palsy and contralateral motor/sensory deficit
○ Bilateral motor/sensory deficit
○ Conjugate eye movement disorder
○ Cerebellar dysfunction (ataxia, nystagmus, vertigo)
Isolated honomymous heminapia or cortical blindness

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42
Q

Haemorrhagic stroke causes

A

HTN, trauma, bleeding disorder, amyloid angiopathy, cocaine, amphetamines, vascular malformations, bleeding into tumours, aneurysmal rupture and vasculitis.

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43
Q

Investigation of stroke risk

A
  • Carotid doppler for atherosclerosis (size of plaques, degree of stenosis)
    Echocardiogram/24h holter (AF, mitral valve disease, cardiac thrombus or valve vegetations
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44
Q

Stroke complications

A

Cognitive impairment, MI, HF (through autonomic dysfunction), dysphagia, aspiration pneumonia, UTI, DVT, PE, dehydration, malnutrition, pressure sores, depression, ortopoedic complications/contractures

Large cerebral infarcts can cause death by associated tissue oedema and herniation (malignant MCA syndrome).

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45
Q

Thunderclap headache

A

Acute, builds to max intensity within 5 minutes

Can indicate IC haemorrhage, venous sinus thrombosis, hypertensive encephalopathy, vertebral artery dissection

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46
Q

RF for subarachnoid haemorrhage

A

HTN, PCKD, ehler danlos, NF1, Marfan’s, alcoholism, smoking, clotting abnormality

1.6x more common in women
2x more common in black people

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47
Q

Presentation of subarachnoid haemorrhage

A

Severe headache
May have brief Loc, N&V, meningismus (aseptic meningitis)
May have seizures

Elderly people may present as seizure, confusion and mild headache/focal neurology

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48
Q

Mechanism of subarachnoid haemorrhage

A

normally aneurysmal, but can be AV malformation or cryptogenic, or can be trauma

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49
Q

Complications from subarachnoid haemorrhage

A

rebleed, seizure, vasospasm, hydrocephalus, electrolyte abnormalities, ECG abnormalities (ST depression, T wave inversion -may mimic MI), pulmonary oedema

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50
Q

Initial investigation for subarachnoid haemorrhage

A

CT within 6h (not as good after this)
LP if 12h since presentation (CSF xanthochromic on visual inspection)
CT/MRI angiography if fit for surgery

51
Q

Most common cause of painful CNIII palsy

A

PCA aneurysm

52
Q

acute subdural haemorrhage

A

Symptoms (Loc, low GCS, anisocoria, motor deficit) with 72h
On May have lucid interval,

CT shows hyperdense (white) blood
Needs surgical evacuation

53
Q

subacute SDH

A

occurs over 3-7 days

54
Q

Chronic SDH

A

over 2 weeks. May have subtle signs.
Blood on CT may be dark as older.
May be managed surgicall or conservatively

55
Q

RF for SDH

A

Age (cerebral atrophy and increased venous fragility), alcohol, seizures, anticoagulants, bleeding disorders, head trauma, IC surgery.

56
Q

Complications from SDH

A

Death due to cerebellar herniation, raised ICP, cerebral oedema, recurrent haematoma formation during recovery, seizures, wound infection, subdural empyema, meningitis, permanent neurological/cognitive deficit, coma/vegetative state

57
Q

Meningism

A

Triad of photophobia, headache and nause

58
Q

Signs of meningism

A

Brudinski sign, kernig’s sign, nuchal nigidity

59
Q

Brudinski sign

A

flex neck causes hip flex

60
Q

Kernig’s sign

A

knee extension elicits pain/resistance

61
Q

Nuchal regidity

A

resistance to passive neck flexions

62
Q

Meningitis

A

inflammation of leptomeninges, can be acute, subacute or chronic
Can be infective or not
Can be pyogenic or aseptic

63
Q

Infective meningitis

A

In infectious causes, get localised infection in host, haematogenous seeding and either direct contiguous spread, or retrograde neuronal pathways allowing CNS entry.

64
Q

Meningitis S+S

A

Typically headache, fever and neck stiffness
Also photophobia, N&V, URTI prodrome, seizures, focal neurological symptoms, lethargy, coma, stupor

Signs include pyrexia, non blanching petechiae (meningococcaemia), morbiliform rash with phatyngitis and adenopathy and vesicles (viral), endotoxic shock, Arthritis (N. meningitidis), extracranial infection (sinusitis, otitis media, mastoiditis, pneumonia)

65
Q

Meningitis associated neurological signs

A
  • Impaired consciousness
    • CN palsy (esp 3, 4,6 or 7 - can be through direct damage or from raised ICP)
    • Papilloedema
    • Focal/generalised seizures
    • Focal neurological signs (hemiparesis, dysphasia, hemianopia)
      Sensorineural deafness)
66
Q

Common bacterial meningitis pathogen

A

Streptococcus pneumoniae, neisseria meningitidis (H influenzae and listeria are more in I/compromise, pregnancy, age extremes)

67
Q

common viral meningitis pathogens

A

(enterovirus, HSV, VZV, EBV, mumps, coxsackie)

68
Q

Neisseria meningitidis classical presentation

A

petechial rash, occurs in small epidermics

69
Q

Common themes for streptococcus pneumoniae meningitis

A

skull fracture, ear disease or congenital CNS lesions

70
Q

Investigations for meningitis

A
  • ABCDE
    • Bedside tests (FBC, U&E, LFT, CRP, clotting, blood culture, meningococcal/pneumococcal PCR, lactate, glucose, throat swab (1x virology, 1 x bacteriology). May do stool sample or HIV test? May do throat swap?)
    • Imaging (CT as quick)
      LP (unless signs of raised ICP (focal neurological signs, GCS<12, seizures or papilloedema). Must record opening pressure if patient can lie down to get it (falsely high if patient is sitting up)- perform protein content, cell count, MC+S, glucose (plus serum glucose), vPCR (24-48h)
71
Q

CI LP in meningitis

A

Raised ICP (papilloedema, focal neurological signs, GCS<12,), signs of meningococcal septicaemia, evidence of bleeding risk (platelets <50, INR>1.2), Hx of clotting disorder, rash/infection at LP site

72
Q

Raised LP pressure in meningitis

A

Bacterial meningitis

May also be raised in fungal/TB

73
Q

Normal LP pressure in meningitis

A

Viral (sometimes, fungal/TB)

74
Q

WCC raised in LP for meningitis

A

Bacterial, viral

Mvariable in fungal/TB

75
Q

polymorphs in CSF for meningitis

A

Bacterial

76
Q

Lymphocytes in CSF for meningitis

A

viral, fungal, TB

77
Q

protein increase in CSF for meningitis

A

bacterial (small rise in viral, fungal and TB)

78
Q

Glucose reduced in CSF for meningitis

A

Bacterial (slight decrease in fungal/TB) - normal in viral

79
Q

Turbid CSF in meningitis

A

bacterial

80
Q

Viscous CSF in meningitis

A

viral

81
Q

gram positive intracellular diplococci in CSF for meningitis

A

pneumococcus

82
Q

Gram negative cocci in CSF for meningitis

A

meningococcus

83
Q

ID TB or fungi in CSF

A

Ziel neelson stain for acid fast TB, indian ink for fungi

84
Q

Management of bacterial meningitis

A

Tx with Abx immediately. Use steroids, notify public health

85
Q

Viral meningitis Tx

A

Main symptoms are fever, seizures and change in mental state. Benzo’s useful for seizures, Aciclovir for virus.

CT may be normal in viral encephalitis, MRI often shows changes

86
Q

Cerebral abscesses

A

headache, fever, altered mental status, focal signs/seizures. Often spread from sinus or blood. CSF may not show much so imaging is key

87
Q

Immunocompromise patients with meningitis

A

HIV+, chemotherapy, alcoholism. Can be atypical organisms e.g. toxoplasmosis, cryptococcus, TB, aspergillus)- may not respond to ceftrioxone.

88
Q

Acute complications in bacterial meningitis

A

sepsis, DIC, hydrocephalus, adrenal haemorrhage (waterhouse friderichsen syndrome)

89
Q

Long term complications in bacterial meningitis

A 
brain abscess, seizure disorder, CN palsy, sensorineural hearing loss, atazia
Brain abscess (rare
90
Q

peripheral causes of unilateral facial weakness

A

Ischaemia, bell’s palsy, sarcoidosis, GB syndrome, Lyme disease, otitis media, Ramsay Hunt Syndrome, cholesteatoma, parotid tumour

91
Q

Cholesteatoma

A

keratinising squamous epithelium within the middle ear or in pneumatised areas of temporal bone. The growth expands, promoting bone reabsorption. Patient presents with hearing loss/ tinnitus, chronic/recurrent aural discharge (unresponsive to Abx) - discharge is generally malodorous. Patient may present with otalgia, vertigo, CNVII involvement (weakness or altered taste). Otoscopy typically shows crust in attic space (upper part of middle ear).Most commonly caused by repeated otitis media, but can be congenital (typically see white mass behind intact tympanic membrane) - congenital form is associated with cleft palate, craniofacial abnormality and chromosomal disorders.

92
Q

Sarcoidosis affecting facial muscle

A

chronic granulomatous disorder, unknown aetiology, affecting lungs, skin and eyes but also other organs. Forms non-ceseating granulomas. Generally classed by organ involvement (ststemic, pulmonary, cutaneous, ocular, cardiac, neuro)- neuro causes headaches and seizures.

93
Q

Lyme disease affecting facial muscle

A
  • Lyme disease starts with erythema migrans 1-2weeks. Has constitutional symptoms (flu like prodrome). Often affects CNVII nerve.
94
Q

Bell’s palsy

A

idiopahic. CNVII inflammation at geniculate ganglion, may be due to HSV-1. Causes LMN pathology. No neurological features. Management is by antivirals, steroids and eye care.

95
Q

Ramsay hunt syndrome

A
  • Ramsay hunt is caused by herpes zoster. Reactivates with geniculate ganglion on facial nerve, but can spread to CNVIII, CNV, CNIX and CNX. Causes ipsilateral facial paralysis, ear pain and vesicular rash. Management is with antiviral, oral steroids and analgesia. Prognosis is less good compaired to bell’s palsy
96
Q

myaesthenia gravis

A

Autoantibodies bind to AcH at NMH. Muscles fatigue on exercise. Often associated with other autoimmunes. Diagnosed by Ach autoantibodies. Can have myasthenic crisis where respiratory failure occurs due to respiratory muscle weakness. Needs intubation and ventilation. Management uses acetylcholinesterase inhibition and immunosuppression

97
Q

CNS causes of unilateral facial weakness

A

stroke, brain tumour (primary or metastatic), MS

98
Q

Facial nerve pathway

A

Arises in pons
Travels through IAM
Enters facial canal
Sensory and motor roots fuse (facial nerve proper) and geniculate ganglion forms
Gives off: Greater petrosal (parasympathetic to mucous and lacrimal glands), nerve to stapedius (motor fibres to stapedius in middle ear), Chorda tympani (taste to anterior 2/3 of tongue), parasympathetic fibres to submandibular and sublingual glands

Also has extracranial branch (posterior auricular nerve for muscles around ear) and motor to digastric and stylohyoid

99
Q

Motor branches of CNVII

A

Temporal zygomatic, buccal, marginal mandibular cervical

100
Q

Anterior cerebral artery serves

A

medial surface of cerebral hemisphere

101
Q

middle cerebral artery serservesves

A

2/3s of lateral surface of brain, central branches supply corpus striatum, thalamus and internal capsule

102
Q

PCA serves

A

Corps callosum, occipital/temporal lobes, central branches supply optic radiation, subthalamic nucleus and thalamus

103
Q

CNIII functions

A

somatic to 4/6 extra ocular muscles, levator palpebrae superioris. Visceral motor to pupil constriction.

104
Q

CNIX functoins

A

gives stomatic to stylopharyngeus (swallowing assistance), visceral motor to parotid, special sensory to posterior 1/3 of tongue, general sensation to external ear and pharynx and visceral sensory from carotid body

105
Q

CNX functions

A

gives somatic motor to palatal/laryngeal/pharyngeal swallowing muscles; visceral motor to trachea, bronchi, GI and heart smooth muscle; visceral sensory from same viscera; special sensory from epiglottis/palate, general sensory from auricle and EAM

106
Q

CNI nuclei

A

olfactory epithelium

107
Q

CNII nuclei

A

retinal ganglion

108
Q

CNIII and CNIV nuclei

A

midbrain

109
Q

CNV, CNVI and CNVII nuclei

A

pons

110
Q

CNVIII nuclei

A

vestibular/spiral ganglion

111
Q

CNIX, CNX and CNXII nuclei

A

medulla

112
Q

CNXI nuclei

A

spinal cord

113
Q

Bulbar palsies

A

Medullary, so CNIX, CNX and CNXII LMN lesions

Flaccid, wasted, fasciculating tongue
Dysphagia
Poor uvula elevationQuiet nasal speech
Jaw jer/gag reflex

114
Q

Common causes for bulbar palsy

A

MND (degenerative), brainstem stroke (vascular), GB (inflammatory ), botulism (infective, neoplastic or congenital

115
Q

Pseudobulbar palsy

A

Bilateral UMN lesion of medullary cranial nerves (so mimics LMN lesion).

Can get exagerated jaw jerk, mood disturbance, spastic tongue

Most common causes are MDN (degenerative), vascular (stroke), MS and head trauma

116
Q

MND presentation for bulbar/pseudobulbar palsy

A

Often mixed presentation, fasciculating tongue with brish jaw jerk

117
Q

Frontal cerebral lesion

A

ntellectual impairment, personality change, urinary incontinence, hemiparesis and Broca’s aphasia (if left frontal)

118
Q

Left temporo-parietal lesions

A

agraphia, alexia, acalculia, Wernicke’s aphasia, contralateral sensory neglect

119
Q

Right temporo-parietal lesions

A

face blindness, cotralateral sensory neglect

120
Q

Cerebellar lesion stmptoms

A
  • Broad ataxic gate (assess with heel-toe walk and Romberg’s test for sensory ataxia)
    • Titubation (rhythmic head tremor)
    • Dysarthria (slurred, staccato speech - Baby hippopotamus/british constitution
    • Nystagmus
    • Dysmetric saccades
    • Upward drift (as per pronator drift but arms move up)
    • Rebound phenomenon (eyes closed, arms raised, push arm down as patient resists - arm shoots up)
    • Hypotonia (decreased in pure cerebellar disease)
    • Mild hyporeflexia
    • Dysmetria (finger to nose)
      Dysdiadochokinesis
121
Q

Causes of cerebellar dysfunction

A

alcohol, drugs (phenytoin), paraneoplastic cerebellar degeneration (seen in breast cancer and small cell lung cancer), severe hypothyroidism
Unilateral defect in MS, stroke, tumours (acoustic neuroma, meningoma)

122
Q

Basal ganglia lesions

A
  • Braadykinesia
    • Muscle rigidity
    • Tremor
    • Athetosis (writhing of face/hands/tongue)
    • Chorea
      Hemiballismus (violent involuntary movements, proximal muscles of 1 arm)
123
Q

UMN lesion causes

A

VINDIE (vascular - stroke, inflammatory - MS/MSN, neoplastic, Degenerative - parkinson’s, Infective - post meningitis, extra (drugs)

124
Q

LMN lesion causes

A

NMJ (MG), peripheral nerve pathology, ventral horn pathology (MND/post polio), muscular pathology

CP1 revision (16 decks)

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