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Neurology > Brain Lesions > Flashcards

Brain Lesions Flashcards

1
Q

Frontal lesion Characteristics

A

Intellectual impairment
Personality change
Urinary incontinence
Monoparesis or hemiparesis

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2
Q

Frontal left lesion characteristics

A

Brocas aphasia

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3
Q

Temporo-parietal left characteristics

A

Acalculia
Alexia
Agraphia
Wernickes
Right-left disorientation
Homonymous field defect

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4
Q

Temporal right lesion characteristics

A

Confusional states
Failure to recognise faces
Homonymous field defect

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5
Q

Parietal lesion characteristics

A

Contralateral sensory loss or neglect
Agraphaesthesia
Homonymous field defect

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6
Q

Parietal right lesion characteristics

A

Dressing apraxia
Failure to recognise faces

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7
Q

Parietal left lesion characteristics

A

Limb apraxia

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8
Q

Occipital / occipitoparietal lesion characteristics

A

Visual field defects
Visuospatial defects
Disturbances of visual recognition

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9
Q

Frontal lesion complications

A

Partial seizures
Focal motor seizures of contralateral limbs
Conjugate deviation of head and eyes away from lesion

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10
Q

Temporal lesion complications

A

Formed visual hallucinations
Complex partial seizures
Memory disturbances

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11
Q

Parietal lesion complications

A

Partial seizures - focal sensory seizures of contralateral limbs

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12
Q

Parieto-occipital lesion complications

A

Crude visual hallucinations

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13
Q

Occipital lesion complications

A

Visual disturbances

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14
Q

Left front-temporo-parietal region disorder of lesions

A

Spoken language - aphasia
Writing - agraphia
Reading - acquired Alexia

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15
Q

Brocas aphasia

A

Damage in left frontal lobe

Reduced speech fluency with relatively preserved comprehension.

Tries to initiate language but becomes reduced to a few disjointed words with failure to construct sentences.

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16
Q

Wernickes aphasia

A

Left trmporo parietal damage

Fluency of language but words are muddled.

Insertion of a few incorrect or non-existent words into speech to a profuse outpouring of jargon.

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17
Q

Nominal - anomic - aphasia

A

difficulty in naming objects.

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18
Q

Global - central - aphasia

A

Combination of brocas and wernickes resulting in loss of language production and understanding

Most common after a severe left hemisphere infarct

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19
Q

Dysarthria

A

Disordered articulation - slurred speech.

Language is intact

Paralysis, slowing or incoordination of the muscles causes various patterns.

e.g. jerky, ataxic speech of cerebellar lesions or hypo phonic monotone of parkinsons.

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20
Q

Lesion in the non-dominant hemisphere

A

Normally the right

Abnormalities in perception of internal and external space - e.g. loss of the way in a familiar surrounding or putting clothes on incorrectly.

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21
Q

Processes of memory

A

Learning
Storage
Subsequent retrieval of learned information

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22
Q

Explicit memory

A

Episodic - recall events

Semantic - recall word knowledge meaning

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23
Q

Implicit memory

A

not conscious - procedural memory - Learning how to ride a bike.

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24
Q

Causes of amnestic syndrome

A

Dementia
Amestic mild congnitive impairment
Alcohol
Head injury
Anoxic brains damage
Stroke
Viral, paraneoplastic or autoimmune encephalitis
Bilateral invasive tumours
Hypoglycaemia
Temporary amnesia

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25
Q

CNI main action

A

Smell

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26
Q

CNII main action

A

vision, fields, afferent light reflex

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27
Q

CNIII main action

A

Eyelid elevation
Eye elevation
Adduction
Depression in abduction
Efferent pupil light reflex

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28
Q

CNIV main action

A

Eye intorsion
Depression in adduction

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29
Q

CNV main action

A

Facial and corneal sensation
Mastication muscles

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30
Q

CNVI main action

A

eye abduction

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31
Q

CNVII main action

A

Facial movement
Taste fibres

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32
Q

CNVIII main action

A

Balance and hearing

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33
Q

CNIX main action

A

Sensation - soft palate and taste fibres

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34
Q

CNX main action

A

Cough
Palatal and vocal cord movements

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35
Q

CNXI main action

A

Head turning
Shoulder shrugging

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36
Q

CNXII main action

A

Tongue movement

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37
Q

Innervation of CNI

A

Olfactory receptors within the nasal mucosa
Pierce cribriform plate and synapse at olfactory bulb
Olfactory tract goes to olfactory cortex

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38
Q

Anosmia causes

A

Head injury - shearing of olfactory neurones as they pass through cribriform plate at skill base

Tumours of olfactory groove - meningioma

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39
Q

Anatomy of CNII

A
  1. Light regulated by papillary aperture converted into action potential by retinal rod, cone and ganglion cells.
  2. Lens under control of ciliary muscle, produces inverted image on retina.
  3. Axons in optic nerve decussate at optic chiasm and fibres from the nasal retina cross and join uncrossed fibres originating in the temporal retina - forming optic tract
  4. Each optic tract carries information from contralateral visual hemifield
  5. From lateral geniculate body, fibres pass in the optic radiation through parietal and temporal lobes to reach visual cortex of occipital lobe.
40
Q

Complete optic nerve lesion

A

Mononuclear field loss on the same side.

Loss of pupillary light reflex

41
Q

Chiasmal lesion

A

Bitemporal hemianopia

42
Q

Optic tract lesion

A

homonymous hemianopia on the same side as lesion

43
Q

Parietal lesion

A

Homonymous quadrantopia
Lower opposite side of lesion

e.g. lesion of RHS
affects lower left segment of eye

44
Q

Temporal lesion

A

Homonymous quadrantopia
Upper opposite side of lesion
E.g. Lesion on RHS affects upper left quadrant

45
Q

Occipital cortex or optic radiation lesion

A

Homonymous hemianopia with macular sparring

46
Q

Occipital pole lesion

A

Homonymous hemianopia - hemiscotoma

47
Q

Examination findings optic neuropathy

A

Reduced acuity in affected eye
A scotoma
Impaired colour vision
Afferent pupillary defect
Optic atrophy - pale disc

48
Q

Causes of optic neuropathy

A

Inflammatory (optic neuritis)
Optic nerve trauma or compression
Toxic
Ischaemic optic neuropathy - GCA
Hereditary
Nutritional deficiency - B1 and B12
Infection
Neurodegenerative disorders
Papilloedema

49
Q

Papilloedema and symptoms

A

Swelling of optic disc
Pinkness, blurring and heaping up of disc margins - nasal first

Underlying disease is most often cause of pt symptoms

Loss of spontaneous pulsation of retinal veins within disc and disc engorged with dilated vessels.

50
Q

Disc infiltration

A

Raised margin swelling e.g. caused by leukaemia

IV flurescein angiography is diagnostic.

51
Q

Causes of optic disc swelling

A

Papilloedema
Brain tumour abscess of haemorrhage
Intracranial HTN
Optic nerve disease
Optic neuritis
Ischaemic optic neuropathy
Orbital mass lesions
Thrombosis
Leukaemia, sarcoidosis, optic nerve glioma via disc infiltration

52
Q

Optic neuritis features and symptoms

A

Most common causes of subacute visual loss

Mild fogging of central vision with colour desaturation to a dense central scotoma.

Pain one eye movements.

53
Q

Causes and Ix of Optic neuritis

A

Plaque of demyelination within the optic nerve

MRI of optic nerve may show additional inflammatory lesions - inc chance of MS

Management = high dose IV steroids acutely

54
Q

Anterior ischaemic optic neuropathy

A

Anterior part of optic nerve supplied by posterior ciliary arteries - so occlusion of hypo perfusion leads to infarction of all or part of optic nerve head

Sudden or stuttering altitudinal visual loss - normally lower half visual field - with disc swelling then optic atrophy

55
Q

Optic atrophy

A

disc pallor, from loss of axons, glial proliferation and decreased vascularity.

May develop to damage axons extensively .

56
Q

Common causes of optic chasm compression

A

Pituitary tumour
Meningioma
Craniopharyngioma

57
Q

Anton syndrome

A

Cortical blindness

Pt cant see but characteristically lacks insight into this - and they may even deny it but pupillary responses remain normal.

58
Q

Physiological anisocoria

A

Slight difference in size of each pupil (up to 1mm)

59
Q

Afferent pupillary defect

A

Optic nerve lesion causes a dilated pupil and an APD:

Left APD:
Unreactive to light
Consensual reflex absent -
If light shone into left eye - right pupil does not restrict but if shone into right eye then left eye will constrict.

60
Q

Relative afferent pupillary defect

A

Incomplete damage to one optic nerve

Left RAPD:
- Direct and indirect reflexes are intact in each eye but differ in relative strength

  • When light is swung left pupil will dilate when illuminated and constrict when right eye is illuminated as consensual reflex is stronger than direct
61
Q

Physiology of pupillary light reflex

A
  1. light activates optic nerve axons via afferent pathway
  2. axons - pass through each lateral geniculate body
  3. synapse at pretectal nuclei

Efferent pathway:

  1. AP pass to edinger-westphal nuclei of IIIrd nerve
  2. Via parasympathetic neurones in 3rd nerve causes pupil constriction
62
Q

Horner syndrome pathophysiology

A

Sympathetic nerve supply

Originates in hypothalamus and descending by way of brainstem and cervical cord

to T1 nerve root, paravertebral sympathetic chain, and on the carotid artery wall to the eye.

Damage to any part of pathway results in horners

63
Q

Clinical features of Horner syndrome

A

Unilateral mitosis - constricted pupil most easily seen in low light

Partial ptosis

Loss of sweating on the same side

Possible subtle conjunctival injection and enopthalmos

64
Q

Myotonic pupil

A

dilated, irregular pupil and more frequent in women.

Unilateral and is common.

No reaction to bright light and also incomplete construction to convergence due to denervation in the ciliary ganglion of unknown cause and has no other path significant.

65
Q

Argyll robertson pupil

A

Small and irregular and rarely seen.

Fixed to light but constricts on convergence

Lesion in brainstem surrounding aqueduct of sylvius

neurosyphillis, diabetes or MS

66
Q

Control of eye movements

A

Fast voluntary eye movement originate in frontal lobe.

Fibres descend and cross in the pons to end in the centre for lateral gaze - (paramedic pontine reticular formation PPRF)

Also receives input from Ipsilateral occipital cortex and Vestibular nuclei

Conjugate lateral eye movement - coordinated from PPRF via medial longitudinal fascicules.

Pass the ipsilateral VI nucleus (lateral rectus) and having crossed the midline to opposite IIIrd nerve nucleus (medial rectus) via MLF - links eyes for lateral gaze.

67
Q

vestibular nuclei

A

linking eye movement with position of head and neck

68
Q

ipsilateral occipital cortex

A

tracking objects

69
Q

Left frontal destructive lesion

A

leads to failure of conjugate lateral gaze to the right

Destructive lesion on one side allows eyes to be driven by the intact opposite pathway

70
Q

Acute lesion

A

Eyes deviated to the side of the lesion, past the midline and look towards the left - (normal limbs) and normally a contralateral right hemiparesis.

71
Q

Intranuclear opthalmoplegia

A

Damage to one MLF

frequently seen in MS

Right INO - lesion of right MLF and on attempted left lateral gaze, right eye fails to adduct or does so slowly.
With left eye develops nystagmus in abduction

Side of lesion is on the side of impaired adduction - not on the side of the obvious unilateral nystagmus.

72
Q

Nystagmus

A

Rhythmic oscillation of eye movement - sign of disease in the retina, cerebellum and or vestibular systems and their connection.

Either jerk or pendular.

73
Q

Jerk nystagmus

A

Fast slow oscillation
seen with vestibular, 8th nerve, brainstem and cerebellar lesions

74
Q

Pendular nystagmus

A

movements to and fro, similar in velocity and amplitude
Usually vertical and present in all directions of gaze

75
Q

CN III physiology

A

lies ventral to the aqueduct in the midbrain and supplies 4 external ocular muscles - SI, MR, IO, and elevator palpbrae which lifts the eyelid.
Affects parasympathetic constriction of pupil

76
Q

Signs of a complete 3rd nerve palsy

A

Unilateral complete ptosis (levator weakness)
Deviation of the eye down and out - unopposed lateral rectus and superior oblique.
Fixed and dilated pupil

77
Q

Difference in diabetic 3rd nerve palsy and posterior communicating artery aneurysm palsy

A

Diabetic is pupil sparing

78
Q

Trochlear IV nerve lesions and physiology

A

Supplies superior oblique
Complains of torsional diplopia when attempting to look down
Head often tilted away from that side

79
Q

Abducens nerve lesions and physiology

A

Supplies lateral rectus muscle for abduction
cause horizontal diplopia when looking into distance with is maximal when looking at the side of the lesion
Eye cannot be fully abducted and an esotropia (inward eye deviation) may be visible

80
Q

Causes of VI palsies

A

damage in brain stem - MS or infarction
Raised ICP
Compression against tip of petrous temporal bone
Nerve sheath infiltrated by tumours - nasopharyngeal carcinoma
Microvascular ischaemia following diabetes that resolves in 3/12

81
Q

Complete external opthalmoplegia

A

immobile eye when 3,4,6 nerve paralysed at the orbital apex - metastasis - or within cavernous sinus - sinus thrombosis or meningioma

82
Q

Pathway of CNV

A

Sensory fibres of the three divisions pass to the trigeminal ganglion ay the apex of the petrous temporal bone. Ascending fibres transmitting light touch enter the 5th nucleus in the pons.
Descending central fibres carrying pain and temperature form the spinal tract of V to end in the spinal 5th nucleus that extends from the medulla into cervical cord.

83
Q

Clinical features of CNV lesion

A

Unilateral sensory loss on the face, scalp anterior to the vertex and the anterior two thirds of the tongue and buccal mucosa

The Jaw deviates to that side as the mouth opens

Diminution of the corneal reflex is an early and sometimes isolated sign.

84
Q

Aetiology of CNV palsies and reasoning

A

Brainstem - infarction etc which may damage nucleus with light touch and spinaothalamic pathways being differently involved

Cerebellopontine angle tumour - compress the nerve and affect VII and VIII nerves producing facial weakness and deafness

Cavernous sinus ans skull based pathology - affect ganglion and proximal branches

Peripheral branches - may be picked off individually

85
Q

Trigeminal sensory neuropathy

A

Gradually progressive, unilateral, facial sensory loss and tingling with normal imaging

Hetergenous in aetiology but may have an autoimmune basis.
Inflammation off the trigeminal ganglion

86
Q

Pathway of the facial nerve

A

sensory taste fibres from the anterior two thirds of the tongue via chord tympani and supplies motor fibres to stapedius muscle

It arises from its nucleus in the pons and leaves the skull through the stylomastoid foramen.

Neurones in each nucleus supplying the upper face (frontalis principally) receive bilateral supra nuclear innervation.

87
Q

UMN lesions CNVII

A

weakness of lower part of face on opposite side. Frontalis is spared.

Normal furrowing of the brown is preserved, eye closure and blinking unaffected.

Earliest sign slowing of one side of face - baring teeth.

88
Q

LMN lesion CNVII

A

Complete unilateral causes weakness ipsilaterally of all facial expression muscles.

Angle of mouth falls with unilateral dribbling developing

Frowning and eye closure weak.

Corneal exposure and ulceration occur if the eye does not close during sleep.

Taste sensation impaired

89
Q

Most common cause of UMN lesion CNVII

A

hemispheric stroke with hemiparesis on the opposite side

90
Q

Pons and causing facial weakness

A

7th nerve loops around 6th nucleus leading to lateral rectus palsy with unilateral LMN facial weakness.

When neighbouring PPRF and corticospinal tract involved there is a combination of :

  • LMN facial weakness
    Failure of conjugate lateral gaze
    Contralateral hemiparesis.
91
Q

Petrous temporal bone and causing facial weakness

A

Nerve may be damaged within the bony facial canal which contains sensory geniculate ganglion.

As well as LMN weakness,

  • Loss of taste to anterior 2/3 tongue
  • Hyperacusis - paralysis of stapedius
92
Q

Causes of petrous temporal bone facial weakness

A

Bells palsy
Trau,a
Middle ear infection
Herpes zoster

93
Q

Pagets disease and CNVII palsies

A

compressed by skull based tumours and may be damaged by parotid gland tumour as the nerve traverses the paretic, and by sarcoidosis and trauma.

94
Q

Bells palsy

A

Due to viral infection or reactivation - herpes simplex

Causing swelling of the nerve within tight petrous bone canal.

Unilateral LMN facial weakness over 24-48 hours with loss of taste or altered on tongue and hyperacusis

Pain behind ear common on onset

95
Q
A

Neurology (10 decks)

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