Brain Lesions Flashcards
Frontal lesion Characteristics
Intellectual impairment
Personality change
Urinary incontinence
Monoparesis or hemiparesis
Frontal left lesion characteristics
Brocas aphasia
Temporo-parietal left characteristics
Acalculia
Alexia
Agraphia
Wernickes
Right-left disorientation
Homonymous field defect
Temporal right lesion characteristics
Confusional states
Failure to recognise faces
Homonymous field defect
Parietal lesion characteristics
Contralateral sensory loss or neglect
Agraphaesthesia
Homonymous field defect
Parietal right lesion characteristics
Dressing apraxia
Failure to recognise faces
Parietal left lesion characteristics
Limb apraxia
Occipital / occipitoparietal lesion characteristics
Visual field defects
Visuospatial defects
Disturbances of visual recognition
Frontal lesion complications
Partial seizures
Focal motor seizures of contralateral limbs
Conjugate deviation of head and eyes away from lesion
Temporal lesion complications
Formed visual hallucinations
Complex partial seizures
Memory disturbances
Parietal lesion complications
Partial seizures - focal sensory seizures of contralateral limbs
Parieto-occipital lesion complications
Crude visual hallucinations
Occipital lesion complications
Visual disturbances
Left front-temporo-parietal region disorder of lesions
Spoken language - aphasia
Writing - agraphia
Reading - acquired Alexia
Brocas aphasia
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.
Wernickes aphasia
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.
Nominal - anomic - aphasia
difficulty in naming objects.
Global - central - aphasia
Combination of brocas and wernickes resulting in loss of language production and understanding
Most common after a severe left hemisphere infarct
Dysarthria
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.
Lesion in the non-dominant hemisphere
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.
Processes of memory
Learning
Storage
Subsequent retrieval of learned information
Explicit memory
Episodic - recall events
Semantic - recall word knowledge meaning
Implicit memory
not conscious - procedural memory - Learning how to ride a bike.
Causes of amnestic syndrome
Dementia
Amestic mild congnitive impairment
Alcohol
Head injury
Anoxic brains damage
Stroke
Viral, paraneoplastic or autoimmune encephalitis
Bilateral invasive tumours
Hypoglycaemia
Temporary amnesia
CNI main action
Smell
CNII main action
vision, fields, afferent light reflex
CNIII main action
Eyelid elevation
Eye elevation
Adduction
Depression in abduction
Efferent pupil light reflex
CNIV main action
Eye intorsion
Depression in adduction
CNV main action
Facial and corneal sensation
Mastication muscles
CNVI main action
eye abduction
CNVII main action
Facial movement
Taste fibres
CNVIII main action
Balance and hearing
CNIX main action
Sensation - soft palate and taste fibres
CNX main action
Cough
Palatal and vocal cord movements
CNXI main action
Head turning
Shoulder shrugging
CNXII main action
Tongue movement
Innervation of CNI
Olfactory receptors within the nasal mucosa
Pierce cribriform plate and synapse at olfactory bulb
Olfactory tract goes to olfactory cortex
Anosmia causes
Head injury - shearing of olfactory neurones as they pass through cribriform plate at skill base
Tumours of olfactory groove - meningioma
Anatomy of CNII
- Light regulated by papillary aperture converted into action potential by retinal rod, cone and ganglion cells.
- Lens under control of ciliary muscle, produces inverted image on retina.
- 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
- Each optic tract carries information from contralateral visual hemifield
- From lateral geniculate body, fibres pass in the optic radiation through parietal and temporal lobes to reach visual cortex of occipital lobe.
Complete optic nerve lesion
Mononuclear field loss on the same side.
Loss of pupillary light reflex
Chiasmal lesion
Bitemporal hemianopia
Optic tract lesion
homonymous hemianopia on the same side as lesion
Parietal lesion
Homonymous quadrantopia
Lower opposite side of lesion
e.g. lesion of RHS
affects lower left segment of eye
Temporal lesion
Homonymous quadrantopia
Upper opposite side of lesion
E.g. Lesion on RHS affects upper left quadrant
Occipital cortex or optic radiation lesion
Homonymous hemianopia with macular sparring
Occipital pole lesion
Homonymous hemianopia - hemiscotoma
Examination findings optic neuropathy
Reduced acuity in affected eye
A scotoma
Impaired colour vision
Afferent pupillary defect
Optic atrophy - pale disc
Causes of optic neuropathy
Inflammatory (optic neuritis)
Optic nerve trauma or compression
Toxic
Ischaemic optic neuropathy - GCA
Hereditary
Nutritional deficiency - B1 and B12
Infection
Neurodegenerative disorders
Papilloedema
Papilloedema and symptoms
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.
Disc infiltration
Raised margin swelling e.g. caused by leukaemia
IV flurescein angiography is diagnostic.
Causes of optic disc swelling
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
Optic neuritis features and symptoms
Most common causes of subacute visual loss
Mild fogging of central vision with colour desaturation to a dense central scotoma.
Pain one eye movements.
Causes and Ix of Optic neuritis
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
Anterior ischaemic optic neuropathy
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
Optic atrophy
disc pallor, from loss of axons, glial proliferation and decreased vascularity.
May develop to damage axons extensively .
Common causes of optic chasm compression
Pituitary tumour
Meningioma
Craniopharyngioma
Anton syndrome
Cortical blindness
Pt cant see but characteristically lacks insight into this - and they may even deny it but pupillary responses remain normal.
Physiological anisocoria
Slight difference in size of each pupil (up to 1mm)
Afferent pupillary defect
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.
Relative afferent pupillary defect
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
Physiology of pupillary light reflex
- light activates optic nerve axons via afferent pathway
- axons - pass through each lateral geniculate body
- synapse at pretectal nuclei
Efferent pathway:
- AP pass to edinger-westphal nuclei of IIIrd nerve
- Via parasympathetic neurones in 3rd nerve causes pupil constriction
Horner syndrome pathophysiology
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
Clinical features of Horner syndrome
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
Myotonic pupil
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.
Argyll robertson pupil
Small and irregular and rarely seen.
Fixed to light but constricts on convergence
Lesion in brainstem surrounding aqueduct of sylvius
neurosyphillis, diabetes or MS
Control of eye movements
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.
vestibular nuclei
linking eye movement with position of head and neck
ipsilateral occipital cortex
tracking objects
Left frontal destructive lesion
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
Acute lesion
Eyes deviated to the side of the lesion, past the midline and look towards the left - (normal limbs) and normally a contralateral right hemiparesis.
Intranuclear opthalmoplegia
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.
Nystagmus
Rhythmic oscillation of eye movement - sign of disease in the retina, cerebellum and or vestibular systems and their connection.
Either jerk or pendular.
Jerk nystagmus
Fast slow oscillation
seen with vestibular, 8th nerve, brainstem and cerebellar lesions
Pendular nystagmus
movements to and fro, similar in velocity and amplitude
Usually vertical and present in all directions of gaze
CN III physiology
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
Signs of a complete 3rd nerve palsy
Unilateral complete ptosis (levator weakness)
Deviation of the eye down and out - unopposed lateral rectus and superior oblique.
Fixed and dilated pupil
Difference in diabetic 3rd nerve palsy and posterior communicating artery aneurysm palsy
Diabetic is pupil sparing
Trochlear IV nerve lesions and physiology
Supplies superior oblique
Complains of torsional diplopia when attempting to look down
Head often tilted away from that side
Abducens nerve lesions and physiology
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
Causes of VI palsies
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
Complete external opthalmoplegia
immobile eye when 3,4,6 nerve paralysed at the orbital apex - metastasis - or within cavernous sinus - sinus thrombosis or meningioma
Pathway of CNV
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.
Clinical features of CNV lesion
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.
Aetiology of CNV palsies and reasoning
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
Trigeminal sensory neuropathy
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
Pathway of the facial nerve
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.
UMN lesions CNVII
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.
LMN lesion CNVII
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
Most common cause of UMN lesion CNVII
hemispheric stroke with hemiparesis on the opposite side
Pons and causing facial weakness
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.
Petrous temporal bone and causing facial weakness
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
Causes of petrous temporal bone facial weakness
Bells palsy
Trau,a
Middle ear infection
Herpes zoster
Pagets disease and CNVII palsies
compressed by skull based tumours and may be damaged by parotid gland tumour as the nerve traverses the paretic, and by sarcoidosis and trauma.
Bells palsy
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
