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STUDY FOR BARRIERS > Neuro > Flashcards

Neuro Flashcards

1
Q

CN 9 does

CN 10 does

A

Carotid BP

Aortic BP

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2
Q

Clinical significance of ACA rupture

A

Subarachnoid haemorrhage
Sits on top of the optic chiasm
Vision problems

Most common place for berry aneurysms

Anterior communicating aneurysm –> visual defects

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3
Q

Most common place for non traumatic intraparenchymal haemorrhage

A

Lenticulostriate arteries off the MCA

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4
Q

Anterior spinal artery supplies

A

Pyramids of medulla
Medial lemniscus of medulla
Nucleus of 12 nerve
Anterior 2/3rds of spinal cord

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5
Q

Derivatives of neural crest cells

A

PNS (peripheral nerve cells, spinal ganglia/autonomic ganglia)

Adrenal medulla

Skin melanocytes

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6
Q

Anomalies in the development of the spinal cord

A

Spina bifida occulta
Meningocele
Myelomeningocele
Rachischisis

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7
Q

The most common site where the neural folds fail to neurulate

A

Cranial neuropore

Resulting in craniorachischisis or anencephaly

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8
Q

What are the parts of the corpus callousum

A

Rostrum
Genum
Body
Splenium

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9
Q

Three parts of the inferior frontal lobe

A

Orbital
Triangular
Opercular

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10
Q

Where is Broca’s area found

A

Inferior frontal gyrus

On the contralateral hemisphere of dominant hand (usually left)

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11
Q

The three types of cortex

A

Archicortex- limbic system
Paleocortex- olfactory bulbs
Neocortex (90%) - cerebral hemispheres

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12
Q

White matter is composed of what types of fibers

A

Association fibers - connect cortical areas in same hemisphere

Projection fibers - connect cortex to subcortical areas (internal capsule)

Callosal fibers (connect cortical areas between hemispheres (corpus callousum, anterior and posterior commisures)

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13
Q

Major components of diencephalon

A

Thalamus (important nuclei include lateral and medial geniculate nuclei for vision and hearing respectively)

Sub thalamus (motor function)

Epithalamus (includes pineal gland, dorsomedial to thalamus)

Hypothalamus (main visceral control system)

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14
Q

What does the hypothalamus control

A

ANS and emotional response together with limbic system
Body temp
Food intake
Water balance
Sleep/awake cycles
Hormones
Control pituitary gland hormone prod (eg growth and cortisol etc)

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15
Q

What does the pineal gland do?

A

Produces anti-gonadotropic hormone and melatonin
Critical for sleep, helps you dream

Removal of gland –> early puberty
Overstimulation –> delayed puberty

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16
Q

What are the parts of the diencephalon?

A 
Thalamus 
Intrathalamic adhesion 
Pineal gland 
Hypothalamus (in the space between third ventricles?) 
Third ventricles 
Mammillary body 
Posterior lobe of pituitary 
Supraoptic recess
Infundibular recess 
Infundibulum
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17
Q

Which layer of meninges forms the blood brain barrier?

A

Arachnoid

And forms the subarachnoid space with CSF and major arteries

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18
Q

Which part of the nervous system do the cranial nerves belong to?

A

All belong to PeripheralNS except CNII (tract of diencephalon)

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19
Q

CN I

A

Olfactory epithelium on superior concha to
Cribiform plate of ethmoid bone to
Olfactory bulb to
Olfactory tract (special sensory and efferent fibers)

Problem–>
Anosmia
Uncinate fits (olfactory hallucinations)

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20
Q

CN II

A 
Retina 
Through optic canals (optic nerve) 
Optic chiasm 
(Optic tract ) 
(Passes pituitary) 
Lateral geniculate bodies

Complications:
Optic neuritis

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21
Q

Visual field defects

A

Bitemporal hemianopsia
(Right) monocular blindness
(Left) homonymous hemianopsia

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22
Q

CN III

A

Motor, parasympathetic
(Sympathetic comes from internal carotid plexus)

Motor: 
Occulomotor nucleus
Cavernous sinus 
Superior orbital fissure 
Muscles (superior medial and inferior rectus, inferior oblique, levator palpebrae superioris "eyelid") 
Parasympathetic : 
Accessory occulomotor nucleus 
Cavernous sinus 
Superior orbital fissure 
Ciliary ganglion 
Short ciliary nerves --> ciliary muscle and sphincter pupillae

Sympathetic*:
Cavernous sinus and superior orbital fissure
(–> branches off as nasociliary nerve –> long ciliary –> dilator pupillae)
(–> to ciliary ganglion –> joins long ciliary nerve

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23
Q

Occulomotor nerve palsy

And causes

A 
Ptosis
No pupillary reflex 
Dilation of the pupil 
Eye abducted 
No lens accomodation

Causes:
Aneurysm of posterior cerebral
Or superior cerebellar artery

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24
Q

CN IV

A 
Motor 
Trochlear nucleus
Cavernous sinus 
Superior orbital fissure 
--> superior oblique

Injury :
Diplopia

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25
Q

Trigeminal nerve branches

A 
Ophthalmic nerve --> 
Lacrimal 
Supratrochlear
Supra-orbital 
Infratrochlear 
External nasal

Maxillary nerve –>
Zygomaticofacial
Infra-orbital nerve ( through infraorbital foramen)
Zygomaticotemporal

Mandibular –>
Mental nerve through mental foramen
Buccal
Auriculotemporal

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26
Q

Course of trigeminal nerve

A

Superior orbital fissure - ophthalmic (foreheads)

Foramen rotundum - V2 (teeth, face)

Foramen Ovale –> mandibular nerve (teeth, chin, muscles of mastication)

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27
Q

CN V1

A

Trigeminal ganglion
Superior orbital fissure (meningeal branch to tentorium cerebelli comes off before this)

–> frontal nerve , nasociliary nerve , lacrimal nerve

Frontal –> one branch to frontal notch (–> supratrochlear) and one to supraorbital foramen (–> supraorbital nerve)

Nasociliary –> long ciliary nerve passes through ciliary ganglion , ethmoidal nerves through anterior/posterior ethmoidal foramen (to ethmoidal and sphenoid foramen)
Nasociliary turns into infratrochlear supplying nasal cavity and side of nose

Sympathetic innervation from carotid plexus –> short ciliary nerves to ciliary muscles via ciliary ganglion

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28
Q

Trigeminal neuralgia

A 
Toothache 
Headache 
earache 
Sinusitis 
Severe neuralgia of unknown causes

Pain can be precipitated by speaking , eating , light touch, draughts on face

Patients can become suicidal because of severe pain

Pain paroxysms in certain sensitive spots for each division
1st - supraoptic notch
2nd - junction of nose and face
3rd - mental foramen

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29
Q

Injury to a given division of trigeminal nerve causes

A

Sensory loss over area supplied

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30
Q

Injury to mandibular nerve

A

Paralysis of muscles of mastication and lower jaw deviates to affected side when mouth is open due to unopposed action of opposite pterygoid muscles

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31
Q

Sensory Reflexes supplied by trigeminal nerve

A 
Corneal reflex (closing eyelid on touching cornea) 
Lacrimal reflex (tears washing eye on irritation) 
Chewing reflex (by presence of food in mouth)  
Sneezing reflex (irritation of nasal mucosa)
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32
Q

Referred pain associated with trigeminal nerve

A

Diseased tooth or cancer of tongue may cause earache or pain radiating up side of head - pain from inferior alveolar nerve or lingual nerve to aurico-temporal

Sever cold on palate - pain over forehead (referred from palatine branches of maxillary division to ophthalmic division)

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33
Q

CN VI

A

Abducent nucleus
Cavernous sinus
SOF
Lateral rectus muscle

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34
Q

Abducent nerve injury

A 
Long intracranial course 
Stretched due to fluid pressure 
Paralysis 
Diplopia- opposite side of lesion 
Aneurysm of Willis 
Septic thrombosis of cavernous sinus
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35
Q

Bell’s palsy

A

Paralysis of facial nerve for no obvious reason
May occur due to exposure to cold or inflammation that occurs near the stylomastoid foramen which compresses the foramen

Inner ear infection
Otitis media

Slight droop in neutral position
Asymmetry on smile
Inability to close eye tightly

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36
Q

Three main types of brain herniation

A

Subfalcine
Transtentorial
Tonsillar

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37
Q

Clinical significance of subfalcine herniation

A

Can compress ACA

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38
Q

Clinical significance of transtentorial herniation

A

CN III compressed –> pupillary dilation and impaired ocular movements on side of lesion

PCA may be compressed –> infarction and further swelling and thus further herniation and Ischemic injury to primary visual cortex

Bigger herniation – can put pressure on midbrain and compress the contralateral cerebellar peduncle against tentorium resulting in ipsilateral hemiparesis (compression creates Kernohan’s notch)

Progression of hernia often accompanied by linear or flame shaped haemorrhages in midbrain and pons termed Duret haemorrhages

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39
Q

Clinical significance of tonsillar herniation through foramen magnum

A

Life threatening
Compressed brain stem
Cardiac and respiratory centres in medulla compromised

40
Q

Cause of bitemporal hemianopia

A

Pituitary adenoma

41
Q

Superior branch of occulomotor nerve supplies which muscles?

A

Superior rectus and levator palpebrae superioris

42
Q

Which nerve does the parasympathetic innervation to the sphincter pupillae and the ciliary muscles

A

CN III

43
Q

What does the inferior branch of CN III supply?

A

Inferior rectus
Medial rectus
Inferior oblique

44
Q

Three main anatomical causes of occulomotor nerve lesion

A

Increasing ICP compresses nerve against temporal bone
Aneurysm of PCA
Cavernous sinus infection or trauma

45
Q

Clinical signs of occulomotor nerve lesion.

A

Dilated pupil
Eyeball in down and out location.
Ptosis

46
Q

Trochlear nerve innervation

A

Contralateral superior oblique

47
Q

Trochlear nerve palsy commonly presents with

A

Vertical Diplopia exacerbated when looking downwards and inwards like when reading or walking down the stairs

Commonly caused by microvascular damage from diabetes or hypertensive. Other causes include thrombophlebitis of cavernous sinus and raised ICP

48
Q

Which branch of trigeminal nerve provides sensory innervation to the lower eyelid ?

A

Maxillary

49
Q

What may be affected by inferior alveolar nerve block?

A

Sensation in the anterior 2/3 of tongue as lingual nerve runs close to the inferior alveolar nerve and may also be affected by local anaesthetic

50
Q

At which point along the course of the facial nerve are the terminal MOTOR branches released?

A

Within the parotid gland

51
Q

Muscles of mastication? Innervated by the trigeminal nerve

A

Medial pterygoid
Lateral pterygoid
Masseter
Temporalis

V3 also supplied the anterior belly of digastric, tensor veli palatini and tensor tympani (derivatives of 1st pharyngeal arch)

52
Q

Corneal reflex

A

Ophthalmic nerve - afferent

Facial nerve - efferent (contraction of orbicularis oculi)

53
Q

Causes of binasal hemianopia?

A

Distension of 3rd ventricle causing pressure on each side of optic chiasm

Atheroma of carotid and posterior communicating artery

Internal carotid aneurysm (?)

54
Q

The lateral rectus muscle takes it origin from

A

Common tendinous ring

55
Q

Palsy of abducens nerve

A

Any pathology leading to downward pressure on the brainstem (eg brain tumour or extradural haematoma)

Other causes include diabetic neuropathy and thrombophlebitis of cavernous sinus but these often affect other nerves as well at the same time

Patient presents with diplopia and a medically rotated eye that cannot be abducted past midline

56
Q

Intracranial Route of facial nerve

A

Nerve arises in pons. It begins as two roots (a large motor root and a small sensory root).
The two roots travel through IAM (part of temporal bone where they are in very close proximity to the inner ear).
Leave IAM and enter into facial canal (Z shaped structure)
Within facial canal - two roots fuse, form geniculate ganglion, give rise to: greater petrosal nerve(PNS of glands), nerve to stapedius and chords tympani

Exits facial canal thorough stylomastoid foramen (just posterior to styloid process of temporal bone)

57
Q

Extra cranial route of facial nerve

A

Exits skill and nerve turns superiority to run just anterior to outer ear.

First branch is posterior auricular nerve
Then nerve to digastric (posterior belly)
Then nerve to stylohoid (muscle)

Main trunk continues as motor nerve - continues anteriorly and inferiorly into parotid gland (parotid gland is innervated by glossopharyngeal just FYi)

Within parotid gland - five branches split: temporal, zygomatic, buccal, marginal mandibular, cervical
^innervate facial expression muscles

58
Q

The third cranial nerve exits brainstem between which two arteries?

A

Posterior cerebral and superior cerebellar

Aneurysm in either would press upon and damage CN III

59
Q

Two cellular things that happen when creating memory

A 
Dendritic spines 
Axonal sprouting (due to increased activity of axonal growth cones)

–> increased number of synapses

Prolonged synaptic transmission

60
Q

What types of receptors are used for the special senses ?

A

Smell - chemoreceptors
Mouth - same
Hearing - mechanoreceptors
Vision - photoreceptors (rods and cones)

61
Q

Define hyperopia

A

Far sightedness
Eye too short
Can’t see close

62
Q

Near sightedness
Can’t see distance
Eye too long
?

A

Myopia

63
Q

Rods vs cones

A

Rods - high light sensitivity, movement, peripheral vision

Cones - colour and acquity
Centred in fovea centralis of macula

64
Q

What detects linear movement

A

Otolith organs in vestibule in inner ear

Utricle and saccule

65
Q

What embryological structures do the basal ganglia rise from?

A

Telencephalon-
Caudate nucleus
Putamen
Globus pallidus

Diencephalon -
Subthalamic nucleus

Mesencephalon -
Substantia Nigra

66
Q

Meningitis lepto vs pachy

A

Lepto is more in acute and involved Pia and arachnoid

Pachy is more chronic like TB and involves dura mater

67
Q

Common meningitis pathogens

A

NHS
Nisseria
Haemophilus
Strep pneumoniae

Enterococci
Cocksackie
CMV
^gut pathogens

Herpes virus 1 and 2 can travel retrograde back through skin through terminal ganglia through nerves to meninges

68
Q

Breakdown of CNS barriers leading to meningitis

A

Tight junctions
Transcytosis
Paracytosis
Extra cellular and intracellular pathogens (eg tb)

69
Q

Pathophysiology of meningitis - main points

A

Brain tropism pathogens (ECHO)
Rapidly multiplying
Virulent strains - capsule, lipopolysaccharide, pilli
Weak host defences

70
Q

Meningitis leads to

A

Increased protein in subarachnoid space so increased outflow resistance to CSF –> hydrocephalus

Back pressure changes:
Hyperaemia oedema leaky vessels

Raised ICP
–> ischemia –> focal neurological signs (suggest encephalitis)

Inflammation –> adhesions –>
Basal cisterns - hydrocephalus
Interpendicular fossa - cranial nerve palsies, internal carotid stenosis

Septicaemia
Sepsis
Cytokines from inflammatory cells and bugs –> DIC (most common with meningococcal meningitis)

71
Q

Neonate with suggested meningitis - what bugs are common?

A

Group b strep

Gram negatives eg E. coli -K1

72
Q

Immune compromised with meningitis - bugs?

A

Mycobacterium tuberculosis
Listeria monocytogenes
Leptospira interrogans

73
Q

STI meningitis bug ?

A

Treponema pallidum (syphilis)

74
Q

Viral meningitis bugs

A 
ECHO
Enteroviruses (poliovirus) 
Herpes simplex 1 and 2 
CMV, cocksackkie 
Mumps
HIV 
Varicella zoster 
Arboviruses
75
Q

Acute vs chronic meningitis presentation

A 
Acute: 
Lepto 
CSF crammed with polymorphs (neutrophils) 
Massive inflammatory response
Viral, bacterial 
Chronic: 
Pachy
CSF shows lymphocytes and fibrin 
Less inflammation and more adhesions causing thrombosis and nerve palsies 
TB, syphilis, cryptococcal(fungus)
76
Q

Clinical features of meningitis

A 
Fever 
Headache 
Neck and back stiffness 
Photophobia
Nausea and vomiting

Kernig sign and brudzinski sign

Encephalitis:
Talking nonsense - altered level of consciousness
Focal neurological signs
Seizures (convulsions)

Children 
Bulging fontanelle (raised ICP) 
Poor feeding
High pitched cry 
Hypotonic 
Convulsions 
Tripod sitting to prevent stretching of meninges
77
Q

Seen on CT in meningitis

A

Loss of cortical sulci
Inflammed meninges (white on contrast)
May be hydrocephalus (ventricles fused or dilated)
Effacement of cortical sulci

78
Q

Contraindications for lumbar puncture

A

Raised ICP

Bleeding disorders

79
Q

Multiple sclerosis - common first presentation?

A

Visual disturbance (usual resolves)
Plaque in optic nerve (normal CT)
Optic neuritis –> some recover and some get MS

80
Q

Subtypes of MS

A

Relapsing remitting
Secondary progressive
Primary progressive (worst, easiest to diagnose, axon injury increases linearly)
Progressive relapsing (prob damage more axons with each episode)

81
Q

Acute MS attacks managed with

A

Corticosteroids

Disease modifying agent available eg inteferon (slows progressing in some, anti inflammatory, high cost)

82
Q

Orbitofrontal cortex injury

A

Often caused by non penetrating brain injury

Cognitive processes of decision making
Emotion and reward in decision making
Integration of information

Causes: frontal lobe dementia, ADHD, drug addiction, maybe OCD

Leads to disruptive decision making, emotion regulation and reward expectation

83
Q

Multiple sclerosis

A

Autoimmune demyelinating
Caused by a combination of environmental and genetic factors that result in a loss of tolerance to self proteins ((myelin antigens)

84
Q

Genetic risk with MS

A

Significant risk attributable to HLA-DR variants
Esp DR2

Some link to genes encoding receptors for cytokines IL-2 and IL-7?

85
Q

Cells assoc with MS

A

Chronic inflamm cells within and around plaques

Central role for CD4+ T cells (esp Th1 and Th17)
Some contribution from CD8+ T cells and B cells

Toxic effects of lymphocytes, macrophages and their secreted molecules –> axonal injury and sometimes even neuronal death

86
Q

Morphology of MS

A

Plaques - multiple, well circumscribed, slightly depressed, glassy appearing, grey tan, irregularly shaped, commonly around ventricles and also frequent in optic nerves/chiasm and brain stem and asc and desc fibre tracts and cerebellum and spinal cord
Microscopically - sharply defined borders

Active plaque- evidence of ongoing myelin breakdown with abundant macrophages containing myelin debris
Lymphocytes and macrophages present
Axons are relatively preserved
Small active lesions often centred on small veins

Inactive plaques - the inflammation mostly disappears leaving behind little/no myelin. Astrocyte proliferation and gliosis are prominent

87
Q

CSF composition in MS

A

Mildly elevated protein level with increased proportion of immunoglobulin
Sometimes moderate pleocytosis
Further examination of Ig reveals oligoclonal bands
Antibodies have a variety of targets and are markers of disease activity

88
Q

Alzheimer’s disease

A

Insidious onset of inspired higher intellectual function and altered mood and behaviour
Later progression to disorientation memory loss and aphasia (severe cortical dysfunction/atrophy)
(Memory and speech)
Death usually from intercurrent pneumonia or other infections

Peptide called beta amyloid or A-beta
Created when the transmembrane protein APP (amyloid precursor protein) cleaved by enzymes beta-amyloid converting enzyme (BACE) (beta secretase) and gamma-secretase. APP can also be cleaved by alpha-secretase and gamma-secretase which liberates a protein that is non pathogenic

Mutations in APP or in components of gamma-secretase (presenilin 1 or 2)–> familial AD
APP gene on chromosome 21 (link to Down syndrome)

Variant of apolipoprotein E called e4 (ApoE4)
Each allele present increases risk by 4

Large deposits - plaques (elicit neuronal death, local inflamm reaction and further cell injury)
AB also leads to hyperphosphorylation of tau protein –> Tau redistributes from axons into dendrites and cell bodies –> aggregates into tangled –> neuronal dysfunction and cell death

89
Q

Morphology of Alzheimer’s

A

Variable degree of cortical atrophy
Widening of sulci most pronounced in frontal temporal and parietal lobes
Hydrocephalus ex vacuo

Microscopic - plaques (extra cellular) and neurofibrilliary tangles (intracellular)
These can just be in elderly people

90
Q

What makes up the neuritic plaques of Alzheimer’s

A

Focal spherical collections of dilated tortuous silver-staining neuritic processes (dystrophic neurites) often around a central amyloid core

Peripheral has microglial cells and reactive astrocytes

Plaques can be found in hippocampus and amygdala as well as in neocortex (motor and sensory cortices spared until later)

Amyloid core contains AB

Lacking surrounding neuritic reaction - diffuse plaques (typically in superficial cerebral cortex basal ganglia and cerebellar cortex (may represent early stage)

Neurofibrilliary tangles - basophilic fibrilliary structures in cytoplasm that displace or encircle nucleus
Commonly in cortical neuron esp enterorihnal cortex and pyrimidal cells of hippocampus, amygdala, basal forebrain and Raphe nuclei
Abnormally phosphorylated tau
Not specific to AD

91
Q

Parkinson’s disease

A

Tremor
Rigidity
Bradykinesia
Instability

Dopamine neurons
Substantial Nigra (project to striatum)

Alpha-synuclein

Point mutations and duplication of gene encoding alpha-synuclein –> autosomal dominant

Lewy bodies (even in sporadic form) (inclusion containing alpha synuckein)

Two other genetic loci: encode protein Parkin (E3 ubiquitin ligase) and UCHL-1 (recycling ubiquitin enzyme)

Assoc with mutations in protein kinase called LRRK2 (shows tangles (tau) or Lewy bodies)

Familial - assoc with mutations in PARK7 or PINK1 (mitochondrial function)

92
Q

Morphology of PD

A

Pallor of substantia Nigra and locus ceruleus

Microscopic -
Loss of pigmented catecholaminergic neurons (associated with gliosis)
Lewy bodies in remaining neurons (intracytoplasmic eosinophilic round to elongated ) - composed on alpha synuckein and others including ubiquitin and neurofilaments
Lewy neurites (dystrophic neurites with alpha synuckein)

Lewy bodies first appear in medulla then pons then substantia Nigra
Eventually bodies and neurites in cerebral cortex and subcortical areas including cholinergic cells of basal nucleus of Meynert and amygdala

Autonomic dysfunction and behavioural disorders in advance of motor problems - lesions in brainstem

Dementia (Lewy body dementia*)

93
Q

Huntington disease

A

Autosomal dominant
Degeneration of striatum (caudate and putamen)
Dance like
Increased and involuntary jerky movements

Early - forgetfulness and thought and affective disorders

CAG trinucleotide repeat expansions on gene on 4p16.3
Encodes protein Huntingtin.
Normal - 11-34 copies
Toxic gain-of-function mutation
Mutant protein subject of ubiquitination and proteolysis - fragments form large intranuclear aggregates

94
Q

Morphology of huntingtons

A

Brain small and striking atrophy of caudate nucleus and sometimes less so the putamen
Changes develop in medial to lateral direction in caudate and dorsal to ventral in putamen
Globus pallidus may atrophy secondarily
Lateral and third ventricles dilated

Atrophy frequent in frontal lobe, less often in parietal and occasionally entire cortex

The medium sized spiny neurons that release GABA, enkephalin, dynorphin and substance P disappear early

Fibrilliary gliosis (more than usual reaction to neuronal loss)

Remaining neurons show intranuclear inclusions - contain aggregates of ubiquinated huntingtin protein

95
Q

Huntington disease

A

Autosomal dominant
Degeneration of striatum (caudate and putamen)
Dance like
Increased and involuntary jerky movements

Early - forgetfulness and thought and affective disorders

CAG trinucleotide repeat expansions on gene on 4p16.3
Encodes protein Huntingtin.
Normal - 11-34 copies
Toxic gain-of-function mutation
Mutant protein subject of ubiquitination and proteolysis - fragments form large intranuclear aggregates

96
Q

Morphology of huntingtons

A

Brain small and striking atrophy of caudate nucleus and sometimes less so the putamen
Changes develop in medial to lateral direction in caudate and dorsal to ventral in putamen
Globus pallidus may atrophy secondarily
Lateral and third ventricles dilated

Atrophy frequent in frontal lobe, less often in parietal and occasionally entire cortex

The medium sized spiny neurons that release GABA, enkephalin, dynorphin and substance P disappear early

Fibrilliary gliosis (more than usual reaction to neuronal loss)

Remaining neurons show intranuclear inclusions - contain aggregates of ubiquinated huntingtin protein

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