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PPE > Neuro > Flashcards

Neuro Flashcards

1
Q

What covers the central nervous system?

A

Meninges

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2
Q

What covers the components of the peripheral nervous system?

A

Endoneurium
Perineurium
Epineurium

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3
Q

What is the barrier between the central and peripheral nervous systems?

A

The pia mater

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4
Q

What are the two main nerve cell types?

A

Neurones and neuroglia

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5
Q

What are the three main types of neurone?

A

Afferent
Efferent
Interneurone

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6
Q

What are the four main types of neuroglial cell?

A

Astrocytes
Oligodendrocytes
Microglia
Ependymal cells

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7
Q

What determines anatomical and synaptic links between neurones?

A

Genetics

Sensory experience

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8
Q

How is the cerebellum connected to the brainstem?

A

By 3 pairs of cerebellar peduncles

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9
Q

What is the conus medullaris?

A

Tapered end of the spinal cord, giving rise to denticulate ligaments and filum terminale

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10
Q

What are the different meningeal layers?

A 
Endosteal layer of dura mater
Meningeal layer of dura mater
Arachnoid mater
Subarachnoid space
Pia mater
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11
Q

What is the function of the subarachnoid space?

A

Contains vessels and is filled with CSF. It acts as a reservoir for metabolic substrate and cushions against mechanical agitation

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12
Q

What’s the difference between meninges of the brain and of the spinal cord?

A

There’s only one layer of dura mater in the spinal cord but the rest are continuous with those of the brain

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13
Q

What is the notochord?

A

A solid cord of cells formed by prenotochordal cells migrating through the primitive pit

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14
Q

How is the neural tube formed?

A

Notochord stimulates lateral elevation of ectodermal neural plate. The depressed mid region is the neural groove and the neural folds grow towards each other until they meet in the midline, forming the neural tube.

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15
Q

In what direction do the neural folds fuse?

A

Begins in the future cervical region, continuing both cranially and caudally

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16
Q

What happens if the anterior neuropore persists?

A

Anencephaly - incompatible with life

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17
Q

What happens if the posterior neuropore persists?

A

Spina bifida which has various degrees of seriousness

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18
Q

What is the difference between the different types of spina bifida?

A

All involve lack of fusion of spinous processes. In spina bifida oculta, they don’t fuse but there’s no visible cyst and no symptoms. In spina bifida with a meningocoele, there’s herniation of meninges out to underneath the skin whereas in spina bifida with a myelomeningocoele, there’s herniation of meninges and neural tissue (part of spinal cord) out to underneath the skin.

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19
Q

What is rachischisis?

A

Failure of elevation of the neural fold and so failure of neural tube formation. This is incompatible with life.

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20
Q

How can neural tube defects be detected?

A

By raised maternal serum alpha-fetoprotein

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21
Q

How can neural tube defects be prevented?

A

Preconceptual folic acid for three months previous and then folic acid supplements taken throughout the first trimester will reduce risk by 70%

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22
Q

How does the development of the spinal cord differ in terms of size, to that of the vertebral column?

A

At the third month, they’re of equal length but after this point, the vertebral column grows faster than the spinal cord. However, spinal roots still have to exit out of their corresponding intervertebral foramina so they have to grow. As the spinal cord ends at level of L1, cauda equina is formed as spinal nerves grow down past this point to exit the vertebral column.

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23
Q

What nerve roots does the cauda equina consist of?

A

L2-S5+coccygeal nerve

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24
Q

What are the three primary brain vesicles?

A

Prosencephalon (forebrain)
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)

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25
Q

What do the three primary brain vesicles develop into?

A

Prosencephalon develops into telencephalon which forms the cerebral hemispheres, and the diencephalon, which forms the thalamus.
Mesencephalon forms the midbrain
Rhombencephalon forms the metencephalon which forms the pons and cerebellum, and the myelencephalon, which forms the medulla oblongata

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26
Q

Where in the neural tube do flexures form?

A

Cervical flexure is located at junction between the hindbrain and the cephalic flexure is located within the midbrain

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27
Q

How is the ventricular system related to the five secondary brain vesicles?

A

Telencephalon lumen is the lateral ventricle
Diencephalon lumen is the third ventricle
Mesencephalon is the cerebral aqueduct
Metencephalon and myelencephalon are the fourth ventricle

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28
Q

What are the embryological precursors to the dorsal and ventral horns of the spinal cord?

A

Alar and basal plates of the neural tube

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29
Q

What are neural crest cells?

A

Cells of the lateral border of the neural tube. They become displaced and enter the mesoderm where they undergo transition from epithelium to mesenchyme

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30
Q

What are the nervous system derivatives of the neural crest cells?

A 
Parasympathetic ganglia
Sympathetic ganglia
Dorsal root ganglia
Cranial nerve ganglia
Schwann cells
Glial cells
Leptomeninges
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31
Q

What are the derivatives of nerual crest cells in the head, neck and midline?

A

C cells of the thyroid gland
Connective tissue and bones of the face and skull
Dermis of the face and neck
Odontoblasts

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32
Q

What are some miscellaneous derivatives of the neural crest cells? (ie not head, neck, midline or nervous system)

A

Adrenal medulla
Melanocytes
Conotruncal septum of the heart

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33
Q

What’s an example of a condition where one component is affected by neural crest cell migration error?

A

Hirschprungs disease with an aganglionic megacolon

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34
Q

What’s an example of a condition where many components are affected by errors in neural crest cell migration?

A

DiGeorge Syndrome

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35
Q

What are placodes?

A

Patches of thickened ectoderm, found on the developing head

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36
Q

What nerve innervates the inner ear?

A

CN VIII - Vesibulocochlear

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37
Q

How do the otic placodes form?

A

At beginning of week three, there’s thickening of the surface ectoderm in the region of the rhombencephalon (hindbrain)

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38
Q

How do the otic vesicles form?

A

There’s continued thickening of the otic placodes until the eventually invaginate and pinch off, forming the otic vesicles

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39
Q

How do the otic vesicles then develop into distinct parts?

A

Form a dorsal and ventral portion and an endolymphatic sac and duct.
Ventral portion is called the saccule and goes onto develop into the cochlea
Dorsal portion is called the utricle and goes on to develop into the semicircular canals in three planes

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40
Q

What is the embryonic derivation of the ossicles of the ear?

A

Stapes develops from the second pharyngeal arch and its reichert’s cartilage bar
Malleus and Incus develop from the first pharyngeal arch and its Meckels cartilage bar

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41
Q

How do the tympanic cavity and eustachian tube develp embryologically?

A

Derived from the first pharyngeal pouch that extends distally to give the tympanic cavity. However it remains narrow proximally, forming the eustachian tube

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42
Q

What is the innervation of the muscles acting on the middle ear?

A

Tensor tympani is innervated by mandibular branch of the trigeminal nerve
Stapedius is innervated by the facial nerve

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43
Q

What is embryonic origin of the external acoustic meatus?

A

First pharyngeal cleft

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44
Q

How is the ear drum formed?

A

Forms from endodermal lining of the tympanic cavity, fibrous stratum connective tissue and from ectodermal lining of the external acoustic meatus. Epithelium at the base of the meatus proliferates forming a meatal plug that eventually dissolves but epithelial lining contributes to eardrum formation

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45
Q

How are the auricles formed?

A

Originate from the first and second pharyngeal arches with 3 auricular hillocks forming either side of the external meatus. This hillocks eventually fuse

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46
Q

How does positioning of the external ear change in the womb?

A

Start off in the neck region but as the mandible grows, the ears ascend to lie in line with the eyes

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47
Q

What is the sensory innervation of the external ear?

A

CNV - trigeminal nerve

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48
Q

What starts off the embryonic development of the eyes?

A

Outpocketings of the forebrain form in week 4, called the optic vesicles and these grow outwards to make contact with the overlying ectoderm. When the vesicles make contact with the overlying ectoderm (placodes) they induce them to makes changes that begin lens formation

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49
Q

What is the optic cup?

A

A double walled invagination of the forebrain that forms on invagination and pinching off of the lens placode

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50
Q

What initially separates the layers of the optic cup?

A

An intraretinal space that eventually closes

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51
Q

What is the purpose of the choroid fissure?

A

Allows the hyaloid artery to pass through to the inner chamber of the developing eye

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52
Q

How does the pupil form?

A

Lips of the choroid fissure close and the mouth of the optic cup forms a round opening and this is the pupil

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53
Q

Why do colobomas occur?

A

If there’s failure of closure of the choroid fissure

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54
Q

What is the remnant of the hyaloid artery of the eye?

A

The central artery of the retina forms from the proximal portion of the hyaloid artery. The distal portion degenerates

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55
Q

What does the optic cup form?

A

The retina
Iris
Ciliary body

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56
Q

What is the make up of the retina?

A

Has two layers.
Outer pigmented layer
Inner neural layer. Anterior 1/5 of which makes up the inner layer of the iris and the ciliary body. The posterior 4/5 consist of rods and cones and so has a photoreceptive layer with an adjacent supportive layer that’s fibrous and contains nerve axons which converge on the optic stalk

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57
Q

What makes up the iris?

A

Pigmented layer of the retina
Internal layer of optic cup
Mesenchyme between optic cup and overlying ectoderm

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58
Q

What is the ciliary body?

A

A muscular and vascular structure that connects the choroid to the lens

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59
Q

What is the derivative of the mesenchyme that overlies the developing ciliary body?

A

Ciliary muscle

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60
Q

How is the ciliary body connected to the lens?

A

Internally via the suspensory ligament

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61
Q

What are the derivatives of the mesenchyme that surrounds the developing eye?

A

Outer layer is continuous with the dura mater and the optic nerve and goes on to form the sclera
Inner layer goes onto the form the choroid

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62
Q

How does the positioning of the developing eye change?

A

Starts off on the side of the face but moves round to the front as facial prominences grow

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63
Q

What are the features of rubella syndrome that crosses the placenta?

A

Cataracts
Patent ductus arteriosus
Microcephaly

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64
Q

What are the main cerebral branches of the internal carotid arteries?

A

The anterior and middle cerebral arteries

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65
Q

What does the middle cerebral artery supply?

A

Sensorimotor strip

Auditory and language areas in dominant lobe

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66
Q

What effects can occlusion of the middle cerebral artery have?

A

Contralateral paralysis of arm and lower face
Contralateral sensory loss or inattention
Speech loss if dominant lobe is affected

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67
Q

What do the anterior cerebral arteries supply?

A

Medial frontal and parietal lobes

Corpus callosum

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68
Q

What effects can occlusion of an anterior cerebral artery have?

A

Paresis of contralateral leg
Contralateral sensory loss
May be gait, micturition and mental disturbances

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69
Q

What does the posterior inferior cerebellar artery supply?

A

Lateral medulla

cerebellum

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70
Q

What effects can occlusion of posterior inferior cerebellar artery have?

A 
Lateral medullary syndrome 
Ipsilateral face and cranial nerve sensory deficits 
Contralateral sensory loss of torso and extremeties 
Dysphagia
Slurred speech
Ataxia
Vertigo 
Nystagmus
Horner's syndrome
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71
Q

What do the posterior cerebral arteries supply?

A

Posterior parietal cortex
Occipital lobe
Inferior temporal lobe

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72
Q

What effects can occlusion of the posterior cerebral arteries have?

A

Visual field deficits (homonymous hemianopia with macular sparing)
Amnesic syndromes

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73
Q

What is the venous drainage of the cerebral cortex?

A

Drains into external cerebral veins and then the superior sagittal sinus
Into the Transverse sinus, then the lateral sinus and into the internal jugular vein

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74
Q

What is the venous drainage of deep structures of the cerebral hemispheres?

A

Drain into internal cerebral veins, great vein and then the straight sinus

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75
Q

What is the arterial supply of the spinal cord?

A

Have two posterior spinal arteries and one anterior spinal artery

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76
Q

Where does the anterior spinal artery run?

A

From lower brainstem to the tip of the conus medullaris

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77
Q

What make up the leptomeninges?

A

Pia mater and arachnoid mater

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78
Q

What are the four meningeal reflections of the dura mater?

A

Falx cerebri
Tentorium cerebelli
Falx cerebelli
Diaphragma sellae

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79
Q

Where is the falx cerebri?

A

In the longitudinal cerebral fissure, between the two hemispheres

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80
Q

Where is the tentorium cerebelli?

A

Separating the occipital lobes from the cerebellum

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81
Q

Where is the tentorial notch?

A

At the free anterolateral border of the tentorium cerebelli

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82
Q

What is the purpose of the tentorial notch?

A

Allows passage of the brainstem

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83
Q

Where in the falx cerebelli?

A

Inferior to the tentorium cerebelli, partially separating the hemispheres of the cerebellum

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84
Q

Where is the diaphragma sellae?

A

Partially covering the hypophysial fossa of the sphenoid and so the pituitary gland

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85
Q

What is formed by the pia mater at the spinal cord?

A

Denticulate ligaments that secure the cord in the canal

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86
Q

What lobes of the brain rest in the anterior cranial fossa?

A

Inferior and anterior aspects of frontal lobes

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87
Q

What bones is the anterior cranial fossa formed by?

A

Frontal lobe anteriorly
Ethmoid bone in the middle
Body and lesser wings of sphenoid posteriorly

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88
Q

What foramina are contained in the anterior cranial fossa?

A

Anterior and posterior ethmoidal formaina
Foramen cecum
Cribriform foramina

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89
Q

What structures pass through the cribrifom foramina?

A

Axons of olfactory cells

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90
Q

What structures pass through the anterior and posterior ethmoidal foramina?

A

Anterior and posterior ethmoidal vessels and nerves

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91
Q

What bones form the middle cranial fossa?

A

Body and greater wings of the spenoid bone
Squamous parts of the temporal bone laterally
Petrous parts of temporal bone posteriorly

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92
Q

What foramina are contained in the middle cranial fossa?

A 
Optic canal
Superior orbital fissure
Foramen ovale
Foramen spinosum
Foramen rotundum
Foramen lacerum
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93
Q

What structures pass through the optic canal?

A

Optic nerve (CNII) and opthalmic arteries

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94
Q

What structures pass through the superior orbital fissure?

A 
CNVi (opthalmic)
Opthalmic veins 
CNIII
CNIV
CNVI
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95
Q

What structures pass through the foramen rotundum?

A

CN Vii

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96
Q

What structures pass through the foramen ovale?

A

CNViii

Accessory meningeal artery

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97
Q

What structures pass through the foramen spinosum?

A

Middle meningeal artery and vein

Meningeal branch of CNViii

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98
Q

What structures pass through the foramen lacerum?

A

Deep petrosal nerve

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99
Q

What structures rest in the posterior cranial fossa?

A

Cerebellum
Pons
Medulla oblongata

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100
Q

What bones form the posterior cranial fossa?

A

Occipital

Petroud and mastoid parts of the temporal bone anterolaterally

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101
Q

What foramina are contained in the posterior cranial fossa?

A

Foramen magnum
Hypoglossal canal
Jugular foramen

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102
Q

What structures pass through the foramen magnum?

A 
Medulla
Meninges
Spinal arteries
Dural veins 
CNXI
Vertebral arteries
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103
Q

What structures pass through the jugular foramen?

A

CN IX-XI
Internal jugular vein
Inferior petrosal sinus
Sigmoid sinus

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104
Q

What structures pass through the hypoglossal canal?

A

CN XII

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105
Q

What are the main different types of receptor cells?

A

Bare terminals of afferent neurones
Encapsulated nerve ending
Nerve ending with associated specialised cell

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106
Q

What is sensory transduction?

A

The conversion of energy of a stimulus into an electrical signal

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107
Q

How does sensory transduction occur?

A

Stimulus alters the permeability of the membrane of a receptor cell and if sufficient, causes depolarisation. This depolarisation is then propagated to the CNS

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108
Q

What is the role of the thalamus in somatic sensation?

A

All ascending sensory information converges on the ventral posterior complex in the thalamus which then arranges highly organised projections to the cortex and gives crude localisation and discrimination

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109
Q

What is the difference between sensory modality and quality?

A

Sensory modality is the kind of stimulus that a receptor responds to, eg touch, whereas sensory quality is a subtype of the modality, eg fine touch

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110
Q

What is the intensity of the felt stimulus determined by?

A

Rate of action potential stimulus, determined by frequency coding
Also, number of activated receptors

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111
Q

What is the receptive field?

A

The space in which a sensory receptor is located and produces stimuli transduction

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112
Q

How does size of receptive field affect acuity?

A

A reduced receptive field size means increased acuity

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113
Q

What does acuity of sensation depend on?

A

Two point discrimination
Signal convergence
Signal divergence
Lateral inhibition

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114
Q

What is lateral inhibition?

A

The process by which excited neurones reduce the activity of their neighbouring neurones and so disable lateral spread of action potentials. This increases sensory perception and acuity.

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115
Q

What is convergence of a sensory signal?

A

Where many first order neurones synapse with one second order neurone. This reduces acuity

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116
Q

What is divergence of a sensory signal?

A

Where one first order neurone synapses with many second order neurones. This amplifies the signal.

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117
Q

What is two point discrimination?

A

The minimum inter-stimulus distance at which two simultaneously applied stimuli can be perceived as distinct

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118
Q

What is two point discrimination determined by?

A

Receptor density
Receptor field size
Psychological factors

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119
Q

Where is the primary somatosensory cortex?

A

At the post-central gyrus

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120
Q

What is the somatotopic arrangement of parts of the body?

A

From feet - trunk - face is arranged in a medial to lateral direction across the primary somatosensory cortex of the parietal lobe

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121
Q

What is astereognosis?

A

The inability to identify an object by active touch without another sensory input

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122
Q

What are the two different types of sensory adaptation?

A

Rapid or phasic

Slow or tonic

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123
Q

What occurs in cells that are slow adaptors (tonic)

A

These cells respond continuously if there is an adequate stimulus so can still be felt. These are good for information on location/size of a stimulus
Eg in pain receptors

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124
Q

What occurs in cells that are rapid adaptors (phasic)?

A

Rapidly respond to a stimulus but then frequency quickly decreases when stimulus is prolonged. This is good for providing information about any changes in stimulus
eg in touch receptors

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125
Q

What are the ascending tracts?

A

Pathways through which impulses are passed from neurone to neurone until they reach either the sensory cortex or the cerebellum. Carry sensory information

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126
Q

What kind of sensation is the medial lemniscal tract responsible for?

A

Fine touch and conscious proprioception

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127
Q

What kind of receptors are involved in the sensation of fine touch, transmitted by the medial lemniscal tract?

A

Meissner’s corpsucle and hair receptors detect stroking
Pacinian Corpsule detects vibration
Merkel disk detects pressure and ruffini ending detect skin stretching

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128
Q

What kind of receptors are involved in the transmission of conscious proprioception by the medial lemniscal tract?

A

Muscle spindles detecting muscle length and movement
Joint receptors detecting joint movement
Golgi tendon organ detecting muscle contraction

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129
Q

What is the path of the medial lemniscal tract?

A

First order neurone arrives in grey matter of the spinal cord and ascends through either fasciculus gracilis or cuneatus if from lower limb or upper limb respectively. Then synapses and the nucleus gracilis or cuneatus of the medulla
Second order decussates within the medulla and then ascends through the contralateral nucleus gracilis to the thalamus where it synapses
Third order neurone starts at ventral posterolateral nucleus of the thalamus and goes to the primary somatosensory area of the cortex, where it terminates

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130
Q

What type of sensation are the spinothalamic tracts responsible for?

A

Lateral tract is responsible for transmission of pain and temperature
Anterior tract is responsible for transmission of crude touch

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131
Q

What types of receptors are involved in the transmission of pain by the lateral spinothalamic tract?

A

Nociceptors which are free ending afferents. Can detect mechanical, thermal or polymodal pain

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132
Q

What types of receptors are involved in the transmission of temperature sensation by the lateral spinothalamic tract?

A

Thermoreceptors which are free ending afferents

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133
Q

What kind of receptors are involved in the transmission of crude touch by the anterior spinothalamic tract?

A

Mechanoreceptors

These can be free ending afferents or merkel disks

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134
Q

Describe the path of the spinothalamic tracts

A

Enters spinal cord at dorsolateral fasciculus and terminates in the grey matter at laminae 1, 2 and 5.
Second order neurone decussates within the grey matter and ascends up through the contralateral tract to the ventral posterolateral nucleus of the thalamus where it terminates
Thirds order neuron runs from VPL nucleus to the S1 area of the cortex

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135
Q

Which ascending tracts are responsible for conscious sensation?

A

Medial lemniscal
Spinothalamic
Trigeminal

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136
Q

Which ascending tracts are responsible for unconscious sensation?

A

Cuneocerebellar

Spinocerebellar

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137
Q

What type of sensation are the spinocerebellar tracts responsible for?

A

Unconscious proprioception

ie information on movement, muscle contraction, joint position etc

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138
Q

Describe the path of the anterior spinocerebellar tract

A

First order neuron enters spinal cord and synapses within the dorsal horn
Second order neurone decussates within the grey matter and ascends in the contralateral tract. It ascends up through the medulla and pons and then decussates again before terminating at the cerebellum (ipsilateral to its origin)

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139
Q

Describe the path of the posterior/dorsal spinocerebella tract

A

First order neurone enters spinal cord and synapses within the dorsal horn.
Second order neuron ascends through its ipsilateral tract and terminates at the ipsilateral cerebellum

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140
Q

What kind of sensation is the cuneocerebellar tract responsible for?

A

Unconscious proprioception

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141
Q

Describe the path of the cuneocerebellar tract

A

First order neuron enters spinal cord and ascends up through the fasciculus cuneatus to the medulla where it synapses within the nucleus cuneatus.
Second order neuron runs from the nucleus cuneatus to the ipsilateral cerebellum

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142
Q

Describe the ascending tract of the trigeminal nerve

A

First order neuron enters at the level of the pons and synapses at the principal nucleus of the trigeminal complex in the pons
Second order neuron decussates within the pons and ascends alongside the medial lemniscal tract to the ventral posteromedial nucleus of the thalamus, where it synapses
Third order neuron runs from VPM nucleus to the S1 area of the cortex

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143
Q

What is a lower motor neuron?

A

A neuron whose cell body lies in the ventral horn of the spinal cord or in the cranial nerve nuclei of the brainstem and directly innervates the muscle via its axon

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144
Q

What is a motor unit?

A

A single axon and all of the muscle fibres that it innervates

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145
Q

What are the two subtypes of lower motor neuron?

A

Alpha LMN with larger diameter (70micrometers) which innervates the muscle itself ie its force generating extrafusal fibres
Gamma LMN with smaller diameter (30 micrometers) which innervates the intrafusal fibres of the muscle spindle

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146
Q

What is a reflex?

A

An involuntary, unlearned, repeatable, automatic reaction to a specific stimulus, that doesn’t require the brain

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147
Q

What are the components of a reflex arc?

A 
Receptor
Sensory neuron
Integration centre
Efferent fibre
Effector
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148
Q

What is the muscle spindle?

A

Encapsulated sense organ within the muscle

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149
Q

What is the function of the muscle spindle?

A

Detects extent of muscle contraction by monitoring the length of muscle fibres. Along with its connections to the spinal cord, it is responsible for tendon reflexes

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150
Q

Where does the muscle spindle relay information to?

A

Motor neurones that innervate its synergistic muscles
Interneurons inhibiting antagonist muscles
Cerebellum via dorsal spinocerebellar tract
Somatosensory cortex
Primary motor cortex via medial lemniscal pathways

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151
Q

What symptoms result if the muscle spindle is damaged?

A

Hypotonia
Uncoordination
Tremor
Reduced joint position sense

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152
Q

What does the muscle spindle consist of?

A

Nuclear bag and chain fibres
Gamma motor neurone
Afferent fibres and nerve endings

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153
Q

What is the purpose of the nuclear bag and chain fibres of the muscle spindle?

A

Bag 1 or dynamic fibres are sensitive to rate of change of muscle length
Bag 2 or static fibres are sensitive to absolute muscle length

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154
Q

What do the afferent fibres and nerve endings at the muscle spindle detect?

A

Type 1a are associates with all intrafusal fibres and detect rate of change of muscle length
Type 2a act on polar regions of intrafusal fibres and detect absolute muscle length

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155
Q

Where is the golgi tendon organ located?

A

At the junction between the muscle and tendon

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156
Q

What is the function of the golgi tendon organ?

A

Monitors degree of contraction and relays information to the spinal cord. Can inhibit agonist muscle to prevent excessive contraction

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157
Q

What is the purpose of the muscle stretch reflex?

A

Template neural circuit for all motor circuits and sets motor tone

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158
Q

How does the muscle stretch reflex work?

A

When the muscle stretches, it is detected by the muscle spindle which relays action potentials to the cerebellum and cortex via spinocerebellar or medial lemniscal tracts respectively, and to the motor neurones. Motor neurones are then recruites to keep the muscle at a constant length

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159
Q

What is the function of the corticospinal tracts?

A

Voluntary movement of the body

160
Q

Describe the path of the lateral corticospinal tract

A

Runs from motor, pre-motor and somatosensory cortices, through the internal capsule, through the pons and to the medullary pyramids. It decussates within the pyramids and tracels down to the spinal cord, where it synapses with a LMN in the ventral horn

161
Q

Describe the path of the lateral corticospinal tract

A

Runs from motor, pre-motor and somatosensory cortices, through the internal capsule to the pons and the medullary pyramids. It remains ipsilateral until it reaches the spinal cord, where it decussates and synapses with the same LMN as the lateral corticospinal tract

162
Q

What is the function of the corticobulbar tract?

A

Facilitates voluntary movement of the head, especially extraocular muscles and muscles of facial expression

163
Q

Describe the path of the corticobulbar tract

A

Runs from motor, premotor and somatosensory cortices, through the internal capsule to the brainstem where it terminates at the motor nuclei of the cranial nerves

164
Q

What are the main locations of termination of the corticobulbar tract?

A

In pons at the trigeminal motor nucleus

In medulla at hypoglossal nucleus

165
Q

Which of the extra-pyramidal tracts decussate?

A

Rubrospinal

Tectospinal

166
Q

What is the function of the vestibulospinal tract?

A

Innervates anti-gravity muscles for posture and balance

Coordination of head and eye movements

167
Q

Describe the path of the vestibulospinal tract

A

Originates at the vestibular nucleus in the pons where it descends through the brainstem, to the spinal cord, where it terminates

168
Q

What symptoms occur if there’s damage to the vestibulospinal tract?

A

Ataxia
Postural instability
Positive Romberg’s test
If unilateral, will sway towards affected side

169
Q

What is the function of the tectospinal tract?

A

Coordination of head and eye movements towards a stimulus

170
Q

Describe the path of the tectospinal tract

A

Runs from tectum in the midbrain, where it decussates shortly after, then runs to the spinal cord where it terminates (cervical and upper thoracic)

171
Q

What is the function of the reticulospinal tract?

A

Coordination of locomotion, posture and rhythmic movements
Facilitation and inhibition of voluntary movement
Influences muscle tone

172
Q

What are the two subdivisions of the reticulospinal tract?

A

Medial or pontine tract

Lateral or medullary tract

173
Q

What are the main actions of the pontine reticulospinal tract?

A

Excitation of antigravity extensor reflex

Increases muscle tone

174
Q

What are the main actions of the medullary reticulospinal tract?

A

Excitation of antigravity flexor reflex

Inhibition of extensor reflex

175
Q

Describe the path of the reticulospinal tract

A

Runs from the reticular formation either in pons (pontine) or medulla (medullary) and remains ipsilateral

176
Q

What is the function of the rubrospinal tract?

A

Provides Flexor tone in distal muscles

Coordination of fine movement

177
Q

Describe the path of the rubrospinal tract?

A

Orginates at red nucleus in the midbrain, where it decussates shortly after. Then continues down to cervical and upper thoracic spinal cord, where it terminates

178
Q

What are the five main points of the organisation of the motor system?

A

Planning, initiation and programming of movement
Coordination of movement
Cortical execution by descending tracts
Spinal cord apparatus
Final common pathway for execution at motor unit

179
Q

Where does the intiation of movements originate?

A

Probably in limbic system and desire converted into movement by basal ganglia and cortical projection areas

180
Q

What happens if there’s damage to the basal ganglia and their cortical projection sites in terms of movement?

A

A range of complex movement disorders and the development of abnormal involuntary movements
Altered ability to activate and suppress movements

181
Q

What are the typical signs of a lower motor neurone lesion?

A 
Weakness
Muscle wasting
Hypotonia
Hyporeflexia/areflexia
Fasciculations
182
Q

What may cause a lower motor neurone lesion?

A

Diabetic neuropathy
Peripheral neuropathy
Traumatic injury
Motor neurone disease

183
Q

What are the typical signs of an upper motor neurone lesion?

A 
Positive babinski
Hyperreflexia
Hypertonia
Spasticity
Clonus
Muscle weakness
184
Q

How does decorticate posturing present?

A

Flexion of arms and wrists
Hands into fists
Feet turned inwards
Extension of legs

185
Q

What are the descending pathway causes of decorticate posturing?

A

Increased rubrospinal and mudullary reticulospinal activity over pontine reticulospinal and vestibulospinal
Disruption of lateral corticospinal activity
Activity of rubrospinal means cannot be decerebrate

186
Q

How does decerebrate posturing present?

A

Extension of arms and legs
Arms and legs internally rotated
Head arched back

187
Q

What are some signs of cerebellar dysfunction?

A 
Ataxia
Dysarthria
Dysmetria
Disequilibrium
Hypotonia
Writer's cramp
Dysdiadochokinesia
Inability to learn new movements
Coarse nystagmus
188
Q

What are the purposes of the three cerebellar peduncles?

A

Superior carries information from the cerebellum to the midbrain
Middle carries information from the cerebral cortex to the cerebellum
Inferior carries information about proprioception to the cerebellum

189
Q

What are the three main functional zones of the cerebellar cortex?

A

Spinocerebellum, in line with the spinal cord
Cerebrocerebellum with its lobes in line with the hemispheres
Vestibulocerebellum inferiorly

190
Q

What are the functions of the three zones of the cerebellar cortex?

A

Spinocerebellum responsible for regulation of body and limb movements, and receives input on proprioception
Cerebrocerebellum involved in planning of movement and motor memory
Vestibulocerebellum Involved in coordinating balance and eye movements

191
Q

What are the structures that make up the basal ganglia?

A 
Putamen
Caudate nucleus
Subthalamic nucleus
Substantia nigra
Globus pallidus
192
Q

What is the purpose of the direct pathway of the basal ganglia?

A

Opens gate for movement initiation

Is excitatory

193
Q

What is the purpose of the indirect pathway of the basal ganglia

A

Antagonises the direct pathway

Is inhibitory

194
Q

What is the function of the basal ganglia?

A

To facilitate the selection of the optimum motor plan by suppressing competing motor plans

195
Q

Describe the direct basal ganglia pathway

A

Cortex wants to carry out a movement so it activates to neostriatum (caudate nucleus and putamen) these are also activates by the substantia nigra. Neostriatum inhibits to SNr and GPi. This removes the usually inhibitory effects of these structures and so inhibition of the thalamus is lifted.
Thalamus can now activate the cortex to carry out movement

196
Q

Describe the indirect basal ganglia pathway

A

Cortex wants to carry out a movement and activates the neostriatum but neostriatum is slightly inhibited by the substantia nigra (SNc)
Neostriatum acts to inhibit the GPe. This lifts its inhibitory action on the subthalamic nucleus. The subthalamic nucleus can now activate the GPi and SNr so the inhibition of the thalamus is increased, and movement is suppressed

197
Q

What basal ganglia structures are under tonic inhibition at rest?

A

Thalamus

Subthalamic nucleus

198
Q

What is the pathology behind parkinson’s disease?

A

Is degeneration of dopamineric neurones of the substantia nigra so there’s reduced activation of the direct pathway so reduced movement. There’s also reduced inhibition of the thalamus at rest so there’s a tremor at rest

199
Q

What are the signs of parkinson’s?

A

Resting tremor
Bradykinesia
Hypertonia

200
Q

What is the pathology behind huntington’s disease?

A

There’s loss of output neurones of the neostriatum and subsequent build up of dopamine. There’s increased inhibition of the subthalamic nucleus and so reduced activation of the GPi and SNr so there’s reduced inhibition of the thalamus so there’s excessive movement of the distal musculature

201
Q

What are the signs of huntington’s?

A 
Uncontrolled movement
Cognitive impairment
Swallowing problems
Slurred speech
Behavioural problems
202
Q

What is nociception?

A

The non-conscious neural traffic orginating with trauma or potential trauma to tissues

203
Q

What are the main different types of nociceptors?

A

High threshold mechanoreceptors that are activated by intense mechanical stimuli
Polymodal nociceptors respond to intense mechanical stimuli, temperature and irritants.

204
Q

What are the different types of nociceptive fibres?

A

Thinly myelinate A-Delta fibres that are rapidly conducting, have a lower threshold and initiate the withdrawing reflex. Associated with high threshold mechanireceptors
C fibres are unmyelinated and indicate there’s tissue damage occurring. Tend to give poor localisation

205
Q

What is the path of second order nociceptive neurones?

A

Descussate in ventral horn and ascend alonside the spinothalamic tracts as the anterolateral system and travel to the brainstem and thalamus

206
Q

What is the general process of nociception?

A

Transduction where nociceptors are activated by a stimulus
Transmission where action potentials are relayed to the CNS
Modulation
Perception

207
Q

What is the pathway for pain sensation of the face?

A

Travels as sensory cranial nerves to pons, medulla, spinal trigeminal complex then synapse and decussate and travel to the brainstem and thalamus

208
Q

What are the two parallel pathways taken in nociception?

A

Direct pathway transmitting physical sensation. Travels to ventral posterior nucleus of thalamus and then to the somatosensory cortex
Indirect pathway for emotional response to pain. Travels to various structures, including the reticular formation, amygdala, peri aqueductal grey matter and hypothalamus, then on to the cingulate and insular cortex

209
Q

How is central modulation of pain carried out?

A

By gate control and descending inhibition

210
Q

What is involved in the gate control theory of pain?

A

Substantia gelatinosa acts to inhibit transmission neurones of pain. Various stimuli can alter this pathway.
Cutaneous stimulation can activate anterolateral neurones but also act to activate the enkephalinergic neurons in the substantia gelatinosa and so reduce pain transmission. ie rubbing a smack.
Tissue damage involves release of mediators such as histamine and prostaglandins. These reduce pain threshold but also act to stimulate C fibres that inhibit the substantia gelatinosa and so activate the pain pathway.
Descending seratonergic pathways can reactivate the substantia gelatinosa and so inhibit pain.

211
Q

What is hyperalgesia?

A

Increased pain at normal threshold stimulation

212
Q

What is allodynia?

A

Pain from stimuli that aren’t normally painful or pain at site that isn’t the stimulated area

213
Q

What is the process behind ‘wind up’ of pain?

A

Tissue or nerve injury leads to persistent pain activation. This causes excessive release of glutamate and increased activation of NMDA receptors. There’s then excessive firing of second order pain fibres and nociceptive neurons become hyperexcitable with responses at lower thresholds and expansion of their receptive fields, leading to allodynia

214
Q

What is neuropathic pain?

A

Pain of neuronal origin and is very difficult to treat as usually can’t be explained by a single disease process. Pain is burning/shooting/tingling and hyperalgesia and allodynia is common

215
Q

How can peripheral nerve injury lead to pain disorder?

A

There’s sensitisation leasing to reduced nociceptor threshold and increased receptive field leading to allodynia, hyperalgesia and hyperpathia. There can be emergence of spontaneous activity and development of abnormal sodium channels that cause inappropriate depolarisations. Afferents can gain access to different spinal regions and transmit high intensity noxious signals instead of low intensity ones

216
Q

What happens in complex regional pain syndrome?

A

Severe continuous burning pain subsequent to injury but doesn’t correspond with normal disease process or lesion of specific root/nerve/trunk. There’s vasomotor changes and oedema, reduced range of motion and trophic changes of hair, skin, nails and muscle

217
Q

What are the different stages of complex regional pain syndrome?

A

Acute with burning throbing pain and localised oedema
Dystrophic with progression of oedema, muscle wasting and other trophic changes
Atrophic with limitation of movement, contraction of digits and waxy trophic changes

218
Q

What are the differences in function and location between rods and cones?

A

Rods are found all around the retina, except for at the fovea centralis. They’re sensitive to low levels of light and so provide night vision. Many rods can converge on a single bipolar neuone
Cones are mainly concentrated at the fovea centralis
They have 3 different types of photo pigments and have a one on one relationship with bipolar cells and so provide colour and high acuity vision

219
Q

What do interneurons of the retina do?

A

Combine signals from photoreceptors and ganglion cells

220
Q

What is the difference between magnocellular and parvocellular pathways for vision?

A

Magnocellular have large receptive fields with no colour selectivity. They run to the posterior parietal cortex and provide information on object location and motion
Parvocellular run to the inferior temporal cortex. They provide fine detail and colour contrast and give information on object recognition and representation

221
Q

Where is the lateral geniculate nucleus?

A

In the thalamus

222
Q

What is the function of the lateral geniculate nucleus in vision?

A

Is location for termination of 90% of retinal axons and gives a retinotopic representation of the contralateral visual field.
It’s where optic tracts converge to form optic radiations.
Gets input from reticular formation, cortex and brain stem so forms feedback connections

223
Q

What is meant by the magnification factor of vision?

A

Fovea centralis has a much higher representation at the lateral geniculate nucleus than the rest of the retina and so there’s increased acuity of it’s areas

224
Q

Describe the path of the optic radiations.

A

From the lateral genicular nucleus, fibres from the inferior part of the retina, giving information on the superior visual field, loop around the temporal horn of the lateral ventricle.
Fibres from the superior half of the retina, giving information on the inferior visual field, wrap around the parietal part of the lateral ventricle

225
Q

How is the primary visual cortex arranged?

A

Into six layers with prominent stripes of myelinated axon white matter. There’s segregation of magnocellular and parvocellular pathways and each cortex represents the contralateral visual field. Most central part of the field is located at the most external part of the cortex

226
Q

What are orientation columns?

A

Structures containing neurones with similar receptive fields of vision

227
Q

What is the function of ‘blobs’?

A

Involved in colour processing

228
Q

Why does vision have a blind spot?

A

As optic disk is the point of exit for the axons of all ganglionic cells so there are so photoreceptors present at this point

229
Q

What are the main symptoms of horner’s syndrome?

A

Miosis
Ptosis
Anhydrosis

230
Q

What is the difference in pathology between closed and open angle glaucoma?

A

In open angle glaucoma, aqueous humour can’t drain through the trabecular meshwork due to degeneration or obstruction
In closed angle glaucoma, aqueous humour can’t reach the trabecular meshwork as iridocorneal angle is closed

231
Q

What is the process behind the blink reflex?

A

CNVi detects tactile stimulation of the cornea and transmits this information to the reticular formation, which activates CNVII which stimulates orbicularis oculi and so the eyelid closes

232
Q

What is the process behind the pupillary light response?

A

Increased light is detected by the retina and information is transmitted to the pretectum. Pretectal neurones are activated by light and transmit information to the Edinger-Westphal nucleus at the midbrain. This transmits parasympathetic signals along to the ciliary ganglion which innervates the sphincter pupillae muscle to constrict

233
Q

What is the process behind the pupillary dark reflex?

A

Fibres run from the retina and the optic tract to the hypothalamus transmitting information about lack of light. This carries sympathetic information to T1-T3 which then travels along the superior cervical ganglion and the long ciliary nerve to dilator pupillae, so pupil dilates

234
Q

What is the process behind the accommodation reflex?

A

Information combines from the lateral geniculate nucleus, retina and visual cortex and visual cortex determines that an image is out of focus and sends corrective signals via the internal capsule.
The supraoculomotor nuclei then generates motor signals for accommodation which bilaterally innervate the oculomotor complex. This innervates medial rectus to converge the eyes.
Edinger westphal nucleus works via CNIII which sends signals along the ciliary ganglion which innervates the sphincter pupillae, ciliary muscle and iris to constrict

235
Q

What is amblyopia?

A

Where one eye doesn’t develop properly and so there’s subnormal development of the visual cortex

236
Q

What are the different types of amblyopia?

A

Strabismic
Refractive
Deprivational

237
Q

What is strabismic amblyopia?

A

Where there’s misalignment of the eyes. Vision in preferred eye will be normal but vision in deviating eye may be abnormal

238
Q

What is refractive amblyopia?

A

Where there’s a difference in the power in each eye

239
Q

What is deprivational amblyopia?

A

Where there was deprivation of vision in early life and so visual cortex didn’t develop properly

240
Q

What is strabismus?

A

A misalignment of eyes, usually due to lack of coordination between extraocular muscles. There’s impairment of binocular vision and depth perception.

241
Q

What are the different classes of strabismus?

A

Exotropia - one eye is turned out
Esotropia - One eye is turned in
Hypertropia - One eye is turned up
Hypotropia - One eye is turned down

242
Q

What kind of lesion could cause a left visual field deficit?

A

Lesion of the left optic nerve

243
Q

What kind of lesion could cause a bitemporal hemianopia?

A

Damage to the optic chiasm eg due to pituitary tumour

244
Q

What kind of lesion could cause a right homonymous hemianopia?

A

Lesion of the left optic tract

245
Q

What kind of lesion could cause a right inferior quadrantanopia?

A

Damage of optic radiations passing through parietal

246
Q

What kind of lesion could cause a right superior quadrantanopia?

A

Damage of optic radiations passing through temporal lobe

247
Q

What are the components of the circle of Willis?

A 
Anterior cerebral arteries
Posterior cerebral arteries
Internal carotid arteries
Posterior communicating arteries
Anterior communicating artery
248
Q

What are the components of the anterior circulation of the brain?

A

Posterior communicating arteries
Internal carotid arteries
Middle cerebral arteries
Anterior cerebral arteries

249
Q

What does the anterior cerebral artery supply?

A

Anteromedial surfaces of the frontal and parietal lobes

250
Q

What does the middle cerebral artery supply?

A

Lateral aspect of frontal, parietal and occipital lobes and sends branches to basal ganglia.

251
Q

What does the posterior cerebral artery supply?

A

Occipital lobe and inferolateral aspect of temporal lobe

252
Q

What does the posterior communicating artery supply?

A

Midbrain and thalamus

253
Q

What does the basilar artery supply?

A

Majority of brainstem

254
Q

What are the main cerebral branches of the internal carotid artery?

A

Opthalamic artery
Anterior choroidal artery
Posterior communicating artery
Continues as middle cerebral artery

255
Q

How are opposite branches of anterior cerebral arteries joined?

A

By anterior communicating artery

256
Q

What are the main branches of the vertebral artery?

A

Spinal artery

Posterior inferior cerebellar artery

257
Q

What arteries are given off by the basilar artery?

A

Superior and anterior inferior cerebellar arteries.

Bifurcates into posterior cerebral arteries

258
Q

What are the functions of the frontal lobe?

A

Motor
Broca’s area for speech
Micturition inhibition

259
Q

What is the function of the parietal lobe?

A

Sensory
Superior optic radiation (inferior defect if damaged)
Angular gyrus for recollection of names/words

260
Q

What is the function of the temporal lobe?

A

Representaion of auditory, vestibular, taste and olfactory functions
Wernicke’s area for speech and comprehension
Memor
Inferior optic radiation (superior defect if damaged)

261
Q

What is the function of the occipital lobe?

A

Vision

262
Q

Describe the blood supply of the spinal cord?

A

Has one anterior spinal artery supply anterior two thirds and paired posterior spinal arteries supplying posterior one third.
Also in lumbosacral region, is anterior artery of adamkiewicz

263
Q

When is there risk of occlusion of anterior spinal artery?

A 
Disease of aorta
Aortic surgery
Vasculitis
Sickle cell disease
Hypotension
Cardiac emboli
Disc herniation
264
Q

What is found on examination in occlusion of anterior spinal artery?

A

Spinal shock with flaccid paralysis, areflexia and anaesthsia
Loss of pain and temperature sensation but retention of dorsal column modalities
Progression to UMN signs

265
Q

If there’s fever associated with occlusion of anterior spinal artery, what may cause be?

A

Acute bacterial meningitis
Epidural/subdural abscess
Granuloma
Viral illness

266
Q

What are differential diagnoses for anterior spinal artery occlusion symptoms (spinal shock, loss of pain and temp. sensation)?

A 
Mass lesion
Intraspinal haemorrhage
Acute exacerbation of demyelinating polyneuropathy
Demylination
Sarcoid
TB
Syphilis
267
Q

How is occlusion of anterior spinal artery managed?

A

Identify cause and treat it
Manage vascular risk factors
Rehabilitate
Prevent complications

268
Q

What is cerebral autoregulation?

A

Process to maintain adequate cerebral blood flow despite changes in cerebral perfusion pressure (if within 60-160) and other stimuli

269
Q

What is cerebral perfusion pressure?

A

Net pressure gradient causing cerebral blood flow to the brain

270
Q

What is a stroke?

A

A clinical syndrome of abrupt loss of focal brain function, lasting for longer than 24 hours, or causing death. Due to either spontaneous haemorrhage into brain substance or inadequate blood supply to a part of the brain

271
Q

What is a transient ischaemic attack?

A

A sudden onset of focal disturbance (may be global) of brain function, presumed to be of vascular origin and completely resolves within 24 hours

272
Q

What are the different origins of an intracerebral haemorrage?

A

May be primary, so no underlying structural problem, lesion or hypertension
May be secondary due to eg a tumour, structural defect of hypertension.
Can also be a haemorrhagic transformation of an ischaemic area

273
Q

What are some possible causes of cerebral infarction?

A 
Large vessel atheroma or embolism
Cardiac embolism
Small vessel disease
Nonatheromatous arterial disease such as arteritis
Blood disorders
Cryptogenic
274
Q

What are some possible causes of intracerebral haemorrhage?

A 
Hypertensive microaneurysms
Lipohyalinosis (arteriolar wall disorganisation)
Anteriovenous malformations or aneurysms
Amyloidangiopathy
Anticoagulants, thrombolytics or thrombocytopenia
Cocaine, amphetamines
Tumour
Venous thrombosis
275
Q

What are the main different classes of stroke?

A

Total anterior circulation stroke
Partial anterior circulation stroke
Lacunar stroke
Posterior circulation stroke

276
Q

What can cause a total anterior circulation stroke (TACS)?

A

Occlusion of proximal internal carotid artery or proximal middle cerebral artery

277
Q

How do total anterior circulation strokes usually present?

A

Contralateral hemiparesis with/without hemianaesthesia
Contralateral hemianopia
Higher cerebral dysfunction

278
Q

What can cause a partial anterior circulation stroke?

A

Occlusion of branch vessel of middle cerebral artery?

279
Q

How do partial anterior circulation strokes present?

A

Either:
2 of hemiparesis, hemianopia, hemianaesthesia
OR
Restricted motor deficit of face, arm or leg
OR
Higher cerebral dysfunction only

280
Q

What can cause a lacunar stroke?

A

Occlusion of a single perforating artery, eg in pons or basal ganglia

281
Q

How do lacunar strokes present?

A

Can be: Pure motor, pure sensory, sensorimotor, or just hemiparesis

282
Q

What happens if there’s occlusion of the posterior inferior cerebellar artery?

A

Lateral medullary syndrome.
There’s loss of pain and temperature sensation of ipsilateral face and cranial nerves, and contralateral trunk and extremeties. Also dysarthria, dysphagia etc

283
Q

How can posterior circulation strokes present?

A

Complex.

May be cranial nerve palsies, sensorimotor deficits, eye movement problems, cerebellar dysfunction

284
Q

What should be assessed when taking a Stroke history?

A

Symptom onset and progression
Neurological symptoms ie location, modalities involved, whether positive or negative
Other symptoms such as headache and seizure suggesting bleeding; headache, vomiting and drowsiness suggesting raised ICP; cardiac symptoms indicating possible cause
Atypical presentations eg with delirium, confucion, collapse, incontinence

285
Q

What are some non-modifiable risk factors for stroke?

A 
Increasing age
Male gender
Genetics
Family history
Previous stroke/ TIA
286
Q

What are some lifestyle risk factors for stroke?

A

Smoking
High alcohol intake
Sedentary lifestyle
Poor diet

287
Q

What are some medical risk factors for stroke?

A

Hypertension
Hypercholesterolaemia
Diabetes mellitus
Arrythmia

288
Q

What are some differential diagnoses for stroke?

A 
Hypoglycaemia
Migrainous aura
Epilepsy
Space occupying lesion
Demyelination
Labyrinthine disorders
Retinal bleeds/infarcts
Peripheral neuropathy
Myopathies
Delirium
Hyperventilation
289
Q

What cortical signs may be seen in stroke of dominant side and non-dominant side?

A

If dominant, may be dysphasia and dysgraphia

If non-dominant, may be neglect and visuospatial disorder

290
Q

What initial investigations should be done when suspecting stroke?

A 
FBC
INR
U+Es, LFTs, glucose, thyroid function tests, lipids
ECG
CT to rule out bleeding/find potential cause 
Carotid ultrasound
MRI later if required
Echocardiogram if required
291
Q

What investigations should be done in cryptogenic strokes/strokes in younger people?

A 
Full coagulation profile and thrombophilia screen
Antiphospholipid antibody screen
Autoimmune screen
Fasting plasma homocysteine
Blood cultures
Syphilis and HIV serology
292
Q

How may stroke be prevented?

A

Antithombotics
Treatment of medical risk factors
Lifestyle changes
Increase compliance with medication

293
Q

What are the different types of cerebral oedema?

A

Vasogenic due to increased capillary permeability
Cytotoxic eg from hypoxia
Interstitial eg in obstructive hydrocephalus

294
Q

What are some causes of raised intracranial pressure?

A 
Tumour
Infection
Haemorrhage
Head injury
Hydrocephalus 
Cerebral oedema
Status epilepticus
295
Q

How does the brain try to compensate for raised intracranial pressure?

A

Reduces cerebral blood flow and so reduces cerebral perfusion pressure. Body detects this and increases systemic blood pressure and dilates cerebral blood vessels causing increased blood volume and increased ICP again

296
Q

What is uncal herniation?

A

Where innermost part of temporal lobe moves towards the tentorium and puts pressure on the brainstem, especially the midbrain

297
Q

What structures are affected in uncal herniation?

A

CNIII so reduced parasympathetic outflow to eye
Ipsilateral posterior cerebral artery so ischaemia of ipsilateral visual cortex so there’s contralateral homonymous hemianopia
Compresses contralateral cerebral crus so there’s ipsilateral hemiparesis
Also decorticate posturing and eventually death

298
Q

What is cingulate herniation?

A

Innermost part of frontal lobe is scraped under the falx cerebri

299
Q

What is tonsillar herniation?

A

Where cerebellar tonsils move down through the foramen magnum compressing the lower brainstem and upper cervical spinal cord

300
Q

What signs are found in tonisllar herniation?

A

Head tilt and neck stiffnes
Flaccid paralysis
BP changes
Respiratory and cardiac dysfunction

301
Q

What are some symptoms of an acute cranial event?

A 
Loss of sensory and motor function
Change in consciousness level/collapse
Abnormal behaviour
Headache
Funny turn
302
Q

How can severity of head injury be assessed?

A

Look at mechanism of injury
Look at signs involved
Look at pattern of change

303
Q

What factors can damage the brain?

A

Lack of substrate
Head injury
Abnormal behaviour ie fitting

304
Q

What are some symptoms of an extradural haematoma?

A 
Unconsciousness followed by a lucid interval and then deterioration
Headache
Nausea and vomiting
Seizure
Bradycardia
Unequal pupils
305
Q

How can an extradural haematoma be treated?

A

Osmotic diuretic

Burr hole for clot evacuation

306
Q

How do subarachnoid haemorrhages tend to present?

A

Thunderclap headache that then diffuses
Vomiting
Seizure
Nck stiffness

307
Q

What are some risk factors for a subarachnoid haemorrhage?

A

Hypertension
Smoking
High alcohol intake

308
Q

How can a subarachnoid haemorrhage be treated?

A

Nimodipine to reduce ischaemia

Surgical clipping if due to aneurysm

309
Q

How do subdural haematomas present?

A 
Loss of consciousness
Anorexia
Vomiting
Neurological deficit
Headache
310
Q

Which groups are at risk of a subdural haematoma?

A

Infants who are physically abused
Elderly with cerebral atrophy
Alcoholics due to cerebral atrophy and increased bleeding time
People on anticoagulants

311
Q

How are subdural haematomas treated?

A

Craniotomy for clot evacuation

312
Q

What are arachnoid cysts?

A

Growths of CSF covered in arachnoidal cells, occurring at arachnoid granulations. Usually congential and slowly developing

313
Q

What are some symptoms of large arachnoid cysts?

A 
Headache
Hydrocephalus
Head deformation
Seizure
Raised intracranial pressure
Ataxia
Hemiparesis
Beahavioural changes
314
Q

How can large arachnoid cysts be treated?

A

Internal or cystoperitoneal shunt
Craniotomy
Drainage by needle aspiration

315
Q

In an ABCD assessment, how should circulation be assessed?

A 
Palpable pulses
Breathing effort
Coughing
Movement
Capillary refill
316
Q

What is the AVPU scale?

A

Way to assess consciousness.
Ranges from:
Alert - Responds to Verbal stimuli - Responds to Painful stimuli - Unresponsive

317
Q

What are the first signs of disturbed consciousness?

A

Change in behaviour and mood
Unsteady on feet
Slurred speech
Difficulty finding words

318
Q

What are some causes of disturbed consciousness?

A

Metabolic eg hypoglycaemia, uraemia, anoxia
Lesions within brainstem or pressure on brainstem due to space occupying lesions in the brain increasing intracranial pressure
Head trauma

319
Q

What is a coma?

A

A state of unrousable unresponsiveness. There’s a lack of a normal sleep-wake cycle and no initiation of voluntary movements

320
Q

When does a coma occur?

A

In diffuse, bilateral cortical dysfunction

Damage to ascending reticular activating system

321
Q

What is delirium?

A

A clinical syndrome involving abnormalities of thought, perception and levels of awareness. Usually intermittent and of acute onset.

322
Q

What can cause delirium?

A 
Acute infection
Post-op
Trauma or head injury
Endocrinopathies
Metabolic
Prescribed drugs
Toxic substances
Vascular disorders
Vitamin deficiencies
Epilepsy
Neoplasia
Urinary retention
323
Q

How can delirium present?

A 
Clouded consciousness, impaired cognition, disorientation
Poor concentration
Memory deficit
ABnormalities of sleep-wake cycle
Abnormalities of perception
Agitation
Emotional lability
Neurological signs
324
Q

What’s the difference between hypoactive and hyperactive delirium?

A

Hypoactive tends to have signs of apathy and quiet confusion, can be confused with depression
Hyperactive tends to have signs of agitation, delusions and disorientation, can be confused with schizophrenia

325
Q

What are some benefits of the glasgow coma scale?

A

Gives a relevant and reproducible assessment of consciousness
Doesn’t require a lot of experience
Gives a global assessment of severity of injury

326
Q

What are the different aspects of the glasgow coma scal?

A

Eye opening 4-1
Motor responses 6-1
Verbal responses 5-1

327
Q

What is the reticular formation?

A

A collection of cells and nuclei throughout the brainstem that receive a wide range of sensory input and provide output throughout the cortex to control the level of conscious awareness of the upper brain so that it can ignore constant background sensory information and stay acutely sensitive to changes in he environment

328
Q

What functions is the reticular formation involved in?

A 
Sleep regulation
Motor control
Cardio and respiratory control
Autonomic functions
Motivation and reward
329
Q

What is the function of the ascending reticular activating system?

A

Transmits information from the reticular formation to the cortex, via the thalamus to increase the level of consciousness.
Filterls incoming signals and provides response via cholinergic neurones in response to a novel stimulus to evoke an output with increased arousal and desynchrony at the cortex

330
Q

What is the activity of the ascending reticular activating system in wakefulness and REM sleep?

A

Projects excitatory information to the thalamus excitatatory neurones and inhibitory information to inhibitory neurones so overall, thalamus is excited, all by ACh neurones. Thalamus then projects excitatory information to the cortex to increase arousal. Cortex also exerts positive feedback on the ARAS and thalamus to further increase arousal

331
Q

What is the activity of the ascending reticular activating system in slow wave sleep?

A

Cholinergic neurons aren’t active in slow wave sleep so don’t project excitatory information to excitatory neurones or inhibitory information to inhibitory neurones/ Therefore, inhibitory neurones are fully active and inhibit the thalamus so there’s reduced projection to the thalamus and there’s little arousal

332
Q

What disorders can arise if the ascending reticular activating system is damaged?

A

Sleep disturbances or coma
Schizophrenia
Parkinson’s PTSD
Altered consciousness

333
Q

Why is sleep necessary?

A

Energy conservation
Convert short term memory into long term memory
CNS resetting/clearance
Homeostasis as bad genes are turned on by lack of sleep

334
Q

What controls the sleep-wake cycle?

A

Reticular formation
Hypothalamus which inhibits the ascending reticular activating system to promote sleep
Biological clock

335
Q

What is parasomnia?

A

Collection of abnormal movements, behaviours, perceptions, emotions and dreams. Commonly occur at junctions between wakefulness and non-REM sleep (hypnogogic) and between REM sleep and wakefulness (hypopompic)

336
Q

What is sleep paralysis?

A

Where person is awake but motor neurones are still being inhibited so there’s paralysis. This is only brief.

337
Q

What is insomnia?

A

A difficulty in initiating or maintaining sleep

338
Q

What are some secondary causes of insomnia?

A

Depression
Personal crises
Old age
Chronic pain

339
Q

What can be used to treat insomnia?

A

Hypnotic medications, such as benzodiazepines but these reduce levels of REM sleep

340
Q

What is hypersomnia?

A

Persistent daytime sleepiness, seen in narcolepsy and obstructive sleep apnoea

341
Q

What are the different types of brain waves seen on an EEG and their frequencies?

A

Beta >14Hz
Alpha 8-13Hz
Theta 4-7Hz
Delta<4Hz

342
Q

When do beta brain waves occur?

A

In arousal. Waves are of very high frequency and are desynchronised

343
Q

When do alpha waves occur?

A

In wakefulness but with eyes closed and in a quiet environment so there’s little stimuli or cortical activity so are of a lower frequency than beta waves

344
Q

When do theta waves occur?

A

In children, concentrating/meditating adults, or at beginning of sleep.
Reduced brain activity so are of lower frequency and more synchronised

345
Q

When do delta waves occur?

A

In deep, slow wave sleep

346
Q

What are the main characteristics of Non-REM or slow wave sleep?

A

Inactive brain but active body. Four stages of differing depth.
Sleep is restorative and endocrine.

347
Q

How does non-REM sleep alter the body’s processes?

A

Reduces cerebral blood flow, oxygen consumption, body temperature, blood pressure and respiratory rate.
It’s point where 95% of pituitary hormones are released and point where 5-HT, NA and ACh are inactive

348
Q

What are the main characteristics of REM sleep?

A

Active brain but inactive body. Similar EEG pattern to arousal and point where dreaming occurs.
There’s a high level of descending inhibition of motor neurones so there’s skeletal muscle paralysis.
Waking most commonly occurs from this point

349
Q

Ho does REM sleep alter bodily processes?

A

Irregular heart and respiratory rate
Penile erection occurs
5-HT and NA are inactive but ACh is active

350
Q

What are the broad definitions of functions of the different layers of the cortex?

A

Layers 1-3 project to other cortical association areas
Layers 1-4 receive inputs from motor and sensory cortices, thalamus and brainstem
Layers 5 and 6 project outputs to hippocampus, basal ganglia, cerebellum and thalamus

351
Q

What is the frontal lobe responsible for?

A 
Motor cortex
Personality and mood
Higher intellect and abstract though
Social conduct
Planning complex movements
Planning for the future
Location of broca's area for language
352
Q

What signs will be found in a frontal lobe lesion?

A

Motor deficits
Personality and behaviour changes
Inability to solve problems
If broca’s area is affected then broca’s aphasia

353
Q

What is the function of Broca’s area?

A

Involved in language, particularly its expression and the translation of thoughts into words

354
Q

What is broca’s aphasia?

A

Also called expressive/motor aphasia. Comprehension is normal but speech is disjointed and there are poorly constructed sentences. May be some motor deficit associated

355
Q

What is global aphasia?

A

Lack of comprehension of spech and written language and inability to form speech, due to extensive broca’s damage

356
Q

What is the parietal lobe responsible for?

A

Primary sensory cortex
Language and calculations in dominant hemisphere
Visuospatial functions and attention in non-dominant hemisphere

357
Q

What will be seen in a parietal lobe lesion?

A

Attention deficit ie contralateral neglect syndrome. Right lobe is predominantly responsible so right lobe lesion will cause severe left neglect and left lobe lesion will cause some right neglect as it will be compensated for.

358
Q

What is the temporal lobe responsible for?

A

Auditory cortex
Memory
Language (wernicke’s area)

359
Q

What is the function of Wernicke’s area?

A

Language and it’s comprehension

360
Q

What will be seen in a temporal lobe lesion?

A

Agnosia which is inability to process sensory information

361
Q

What is wernicke’s aphasia?

A

Also called receptive/sensory aphasia. Is lack of comprehension of language. Speech is fluent but unintelligible/nonsensical

362
Q

What is the function of the limbic associaton area?

A

Attaches emotional connotations to sensory input and consequent behaviour. Rewards good behaviour with positive sensations and punishes socially inept behaviour

363
Q

What is mostly controlled by the dominant hemisphere?

A 
Language
Maths
Logic
Motor skills
Processes information in sequence
364
Q

What is mostly controlled by the non-dominant hemisphere?

A 
Emotion of language
Music and art
Visuospatial
Bodily awareness
Processes information as whole picture
365
Q

What is aphasia?

A

The disturbance of comprehension and expression of language

366
Q

What is conduction aphasia?

A

Intact comprehension and speech production but there’s poor repetition of speech and errors are frequently made in spontaneous speech eg transposition or substitution of sounds

367
Q

What is nominal aphasia?

A

Difficulty in putting names to objects etc but comprehension of what they are and their function is intact

368
Q

What are the two main types of memory?

A

Procedural

Declarative

369
Q

What is procedural memory?

A

Involved in the performance of learnt motor skills. Memories are difficult to form but long lasting and don’t require conscious recollection

370
Q

What structures are involved in procedural memory?

A

Cerebellum
Basal ganglia
Pre motor cortex

371
Q

What is declarative memory?

A

Naming of objects and recognition of places etc. Memories are rapidly learnt and rapidly forgotten and are assessed consciously

372
Q

What structures are involved in declarative memory?

A

Connections between hippocampus and cortex

373
Q

What are the different types of declarative memory?

A

Immediate gives sense of present. Ability to hold a moment in mind for afew seconds.
Short term gives working memory. Can hold an experience in mind for minutes/hours. Allows us to retain information until task is completed
Long term gives information that can be retrieved months/years layter

374
Q

What is meant by long term potentiation of memory?

A

A long lasting enhancement in signal transmission between two neurones, involving NMDA glutamate receptors in hippocampus. Underlies synaptic plasticity

375
Q

What is meant by long term depression of neurons?

A

Weakening of synapses that are infrequently used

376
Q

What would happen if there was damage to the hippocampus?

A

Anterograde amnesia which is inability to form new memories

377
Q

What is retrograde amnesia?

A

Inability to retrieve old memories

378
Q

What is consolidation of memory?

A

Stabilising of a memory after its initial acquisition. Part of conversion of short term memory into long term, through emotion, rehearsal and association

379
Q

What are some possible causes of amnesia?

A 
Vascular interruption
Trauma
TUmour
Infection
Electroconvulsive therapy
380
Q

What happens in cerebral abscess formation?

A

Spread of infection leads to pus accumulation and local tissue destruction with adjacent brain becoming oedematous. A pyogenic membrane forms around the abscess and granulation tissue forms. At this point can only be treated by excision/aspiration

381
Q

What are some complications of a cerebral abscess?

A

Meningitis
Intracranial haemorrhage, raising intracranial pressure
Epilepsy
Focal neurological deficit

382
Q

What happens in encephalitis?

A

Viral infection causes inflammation of the brain parenchyma. There’s infiltration of lymphocytes, plasma cells and macrophages and neuronal cell death wih phagocytosis of debris. There’s then reactive hypertrophy and hyperplasia of microglia and vasogenic oedema

383
Q

What are the symptoms of encephalitis?

A 
Fever
Behavioural changes
Drowsiness
Confusion
Weakness
Seizures
384
Q

What’s a histological marker of alzheimer’s?

A

Amyloid plaques which are foci of enlarged neurones, synaptic terminals and dendrites
Neurofibrillary tangles which are thickening of fibrils in neuronal cytoplasm

385
Q

What is prion related disease?

A

Disease involving mutated prion protein (PrP) which is normally a normal compeonent of the synapse. There’s aggregation of these PrPs and so there’s cell death and holes form in the grey matter (spongiform encephalopathies)

386
Q

Whatis an example of prion related disease?

A

Bovine spongiform encephalopathy and then new variant Creutzfeld Jakob Disease

387
Q

What is the prodromal phase of raised intracranial pressure?

A

Occurs between start of condition and its full expression. There’s headach, vomiting and papilloedema

388
Q

What happens in the acute phase of raised intracranial pressure?

A

COmpression of occulomotor nerve so pupil dilation
Compression of brainstem so coma
Compression of cerebral peduncles so hemiparesis

389
Q

How can diffuse axonal injury occur in head trauma?

A

If microtears occur to axons at points where density of brain substance changes
Tearing of nerves and small vessels
Tearing of pituitary stalk

390
Q

How does diffuse axonal injury heal?

A

By gliotic scarring

391
Q

What are the different types of glial cell?

A

Astrocytes
Microglia
Oligodendrocytes

392
Q

What is the function of astrocytes?

A

Form blood brain barrier
Supply neurones with nutrition
Remove neurotransmitters
Maintain ionic environment of neurone

393
Q

What is the function of oligodendrocytes?

A

Myelinate axons of the CNS

394
Q

What is the function of microglia?

A

Immune function of the CNS. Can become phagocytic when activated

395
Q

What is the function of ependymal cells?

A

Facilitate movement of CSF

Form barrier between CSF, ventricles and neurones, together with astrocytes

PPE (2 decks)

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