Basics & cerebral malformations Flashcards
What are glial cells?
Supporting structure for neurons
Types of glial cells include:
1) microglia (CD4)
- part of the macrophage system
2) astrocytes - most common and found in the grey and white matter. Has many functions include:
- scar formation (gliosis)
- remove neurotransmitters in synaptic clefts
- remove neuronal debris along microglia
- take up KCL released by neurones when there is increased activity
3) oligodendrocytes (found in grey and white matter)
- produces CNS myelin
- it’s peripheral cousin is the schwann cell
4) ependyma
- line ventricular system and extends into central canal of spinal cord
What re the blood supply to the brain?
Internal carotids and basilar artery supply circle of willis
Anterior cerebral artery - frontal lobe and parietal lobe Middle cerebral artery - parietal lobe (speech area) and temporal lobe Posterior cerebral artery - occipital lobe
Vertebrobasilar system supplies cerebellum and brainstem
What is the significance of reappearances of primitive reflexes?
Grasp and rooting reflexes are inhibited by maturation of frontal lobes but may appear later with acquired frontal lobe lesions.
Asymmetry or persistence of primitive reflexes may indicate focal brain or peripheral nerve lesions.
What is the difference between white and grey matter?
Grey matter
- pinkish-grey color in the living body
- continues the cell bodies, dendrites and axon terminals of neutrons
- where all the synapses are
- Distributed at the surface of the cerebrum (cerebral cortex) and of the cerebellum (cerebellar cortex), as well as in the depths of the cerebrum (thalamus; hypothalamus; subthalamus, basal ganglia – putamen, globus pallidus, nucleus accumbens; septal nuclei), cerebellar (deep cerebellar nuclei – dentate nucleus, globose nucleus, emboliform nucleus, fastigial nucleus), brainstem (substantia nigra, red nucleus, olivary nuclei, cranial nerve nuclei).
White matter
- made of axons connecting different parts of grey matter to each other
What makes up the basal ganglia and what is its function?
Basal ganglia contains the caudate nucleus, putamen and globes pallidus.
Situated anterior and lateral to internal capsule
Function
- integration of motor movements
- lesions cause meaningless, unintentional, unexpected contralateral movements
**kernicterus –> build up of bilirubin in basal ganglia –> athetoid CP
What makes up the thalamus and what is its function?
The thalamus includes the hypothalamus, sub thalamus and epithalamus
Functions as integration of information
- info to / from cortex must pass through thalamus
- lesions affect contralateral sensation
Where is the internal capsule and what is its function?
Connect tract between cerebrum and brain stem
Located between the basal ganglia and thalamus
Contains both motor and sensory fibres
Anterior limb
- transmits fibres from frontal lobe
Posterior limb
- transmit corticospinal and corticobulbar tracts
Optic radiation comes off at the back of internal capsule
Sensory fibres pass from cerebrum via the IC to thalamus
Lesions of IC cause contralateral sensory and motor changes
What is the main role of cerebellum?
Proprioception and vibration sense from limbs
Receives sensory information from spinocerebellar tract
Lesion manifest on ipsilateral side
Where are the cranial nerve nuclei?
Brain - I and II Midbrain - III, IV Pons - V, VI, VII, VIII Medulla - Ix, X, XI, XII
What side would cranial nerve lesions affect?
Cranial nerve supple comes from both cerebral cortex
- unilateral abnormality of a cranial nerve implies a lesion at the level of the cranial nerve nuclei or the nerve itself
What cranial nerves are pure motor?
3, 4, 6, 11 and 12
- All divisible into 12 apart from 11
What cranial nerves are parasympathetic?
3, 7, 9 and 10
What is CN II?
Optic nerve
- traves to lateral geniculate body –> optic radiation –> posterior internal capsule –> occipital lobe
How does the light / accomodation reflex work?
Light –> CN II (afferent) –> Edinger Westphal nucleus –> CN III (parasympathetic efferent) –> constriction
No cortical involvement in reflex inteslf
CN II (afferent defect) –> reduced acuity, absent constriction of ipsilateral pupil and dilated consensual response
What are causes of absent light reflex but intact accomodation?
Argyl-Robinson pupil
- small, irregular, unequal pupil
- normal accomodation
- mid brain lesion
- syphilis, diabetes, alcohol
Adie’s pupil
- caused by ciliary ganglion lesion (efferent parasympathetic pathway)
- decreased or absent reaction to light
- slow or incomplete reaction to accomodation
- reduced tendon reflexes
- usually young women
Parinaud’s syndrome
- vertical gaze palsy, sunset sign +/- pupillary or CN III nuclear palsy
- retractile nystagmus, impaired convergence
- classically a/w tumour of pineal or 3rd ventricle
- differential would be trauma / demyelination
Bilateral arterial visual pathway lesions
What are causes of each of these field defects?
- Tunnel vision
- Blind spot
- central scotomata
- unilateral field loss
- bitemp hemianopia
- homonymous hemianopia
- upper quadrantanopia
- lower quadrantanopia
Tunnel vision - glaucoma, papilloedema, syphilus Blind spot - optic nerve head enlargement central scotomata - optic nerve lesion between head and chiasm - demyelination, toxic, vascular, nutritional unilateral field loss - optic nerve lesion bitemp hemianopia - optic chiasm homonymous hemianopia - occipital tract to occipital cortex lesion - may have macular sparing upper quadrantanopia - temporal lobe lesion lower quadrantanopia - parietal lobe lesion
What are the actions of CN III, IV and X?
3, 4, 6 make the eye do tricks!
CN III (oculomotor)
- Innervates superior rectus, medial rectus, inferior rectus, and inferior oblique muscles
- pupil constriction
- levator palpabrae superioris
CNIV (Trochlear)
- superior oblique
- pulls eye down when looking medially
CNVI (abducens)
- lateral rectus
- moves eye laterally
What happens in CN III palsy?
Eye deviate down and out due to unopposed action from CN IV and CN VI
A/w
- ptosis
- pupillary dilation, unreactive to direct light / accomodation
Usually congenital in paediatric population Other causes - birth trauma - central (brainstem) tutor - Aneurysm - inflammatory / infectious - trauma - migraine
What happen in CN IV palsy?
Superior oblique palsy results in weakness of inferior gaze on adduction
- Look up and out
- May tilt head away from lesion to maintain binocular lesion
Most commonly acquired from trauma
What happens in CN VI palsy?
Paresis of lateral gaze
Congenital
- rare
- Aka Duanes’s
Acquired
- a/w hydrocephalus, raised ICP
- trauma
- vasc. malformation
- meningitis
- a/w mastoiditis
What are causes of ptosis?
If normal pupils then it is a muscular problem
- myasthenia gravis
- botulism
- fascioscapulohumeral dystrophy
- thyrotoxic myopathy
If pupil is dilated
- CN III lesion
If pupil is constricted
- Horner’s syndrome
- Tabes dorsalis from neurosyphilis
What controls conjugate gaze?
The medial longitudinal fasciculus
- direction of conjugate gaze is controlled by contralateral side of brain
- i.e if conjugate gaze to right then controlled by left brain
Frontal lobe controls saccadic movement
Occipital lobe controls smooth pursuit
Brainstem co-ordinates gaze
Frontal lobe lesion causes contra-lateral horizontal paralysis
Brainstem lesion causes ipsilateral horizontal gaze paralysis
What does a medial longitudinal fasiculus lesion cause?
Internuclear ophthalmoplegia
- failure of adduction in ipsilateral eye
- nystagmus of abducting eye
How is nystagmus named?
After the direction of rapid phase (which is actually correction of abnormal drift)
What causes the below types of jerky nystagmus?
- vertical (upbeat / downbeat)
- horizontal
Vertical nystagmus
- upbeat: 4th ventricule lesion
- downbeat: foramen magnum lesion
Horizontal nystagmus
- vestibular
- cerebellum
What causes pendular nystagmus?
Retinal or congenital causes
What is horner syndrome?
Aka oculosympathetic paresis
- disruption to the sympathetic nerve trunk
Triad
- Ptosis
- Myosis (constricted pupils)
- Anhydrosis
Need to make sure it isn’t part of lateral medullary syndrome which is
- Horner syndrome
- ipsilateral nystagmus
- ipsilateral CN V, IX, X lesion s
- ipsilateral cerebellar signs
- contralateral pain and temperature over trunk and limbs
What is Duane syndrome?
Most common congenital oculomotor abN
- may be AD or sporadic
- usually unilateral
- due to variation in innervation of affected eye’s lateral rectus muscle
What eye signs do you see with hydrocephalus?
Impairment of vertical gaze and pathological lid retraction (setting sun sign) due to dilation of supra-pineal recess (post. 3rd ventricle), pushing down on midbrain ‘tectum’
What does CN V do?
Trigeminal nerve
- facial sensation and motor supply to muscles of mastication
What does CN VII do?
Facial nerve
- motor function of facial muscle
- taste to ant 2/3 tongue
- UMN provides bilateral innervation of upper and lower facial muscles therefore upper motor nerve facial palsy will result in ipsilateral paralysis of lower facial muscles contralateral only (i.e facial droop in stroke)
- Lower motor neurone facial nerve –> ipsilateral paralysis of facial muscles
What does the CN VIII do?
Vestibulococholear nerve
- Palsy results in vertigo and absent cold caloric testing
If the lesion is in the brain stem and affects the cochlea nucleus only the only symptom is deafness
What is the weber / rinne test for?
Weber
- tuning fork in the middle of the forehead
- if sensorineural hearing loss, side affected can’t hear
- if conduction hearing loss, affected side louder
Rinne
- tune fork in front of ear vs mastoid
- normal is louder in front than bone (positive rinne)
- If sensorineural hearing loss, both will be down
- If conduction hearing loss, negative rinne