Neuroscience & Mental Health Flashcards

1
Q

What are the divisions of the brainstem?

A

Midbrain, Pons and Medulla oblongata

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2
Q

What is not a bilateral structure on the posterior brainstem?

A

Pineal Gland

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3
Q

What do the four colliculi do?

A

The superior colliculi are important for head and neck reflexes related to VISION
The inferior colliculi are important in AUDITORY reflexes.

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4
Q

What cranial nerve(s) emerge from the dorsal brainstem?

A

Trochlear Nerve (IV)

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5
Q

What connects the cerebellum to the brainstem and how.

A

Cerebellar Peduncles.
Superior peduncle to midbrain
Middle peduncle to pons
Inferior peduncle to medulla

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6
Q

What ascending pathways are visible in the posterior brainstem?

A

Dorsal columns to the thalamus

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7
Q

What cranial nerves do not arise from the brainstem, and what are their function(s)?

A

CN 1 - Olfactory Nerve: contains afferent nerve fibres of the olfactory neurones to the CNS. Originates from cerebrum.
CN 2 - Optic Nerve: transmits visual information from the retina to the brain. It originates from the diencephalon.

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8
Q

What cranial nerves arise from the midbrain, and what are their function(s)?

A

CN 3 - Oculomotor: allows movement for the eye and eye-lid. It arises from the interpeduncular fossa.
CN 4 - Trochlear Nerve: smallest cranial nerve, innervating only the superior oblique muscle of the eye.

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9
Q

What cranial nerves arise from the pons/pontine-medullary junction, and what are their function(s)?

A

CN 5 - Trigeminal Nerve: largest cranial nerve and is composed of three major branches, responsible for sensation in the face and major functions like chewing.
CN 6 - Abducens Nerve: somatic efferent that controls the movement of the lateral lecture muscle. Arises most medially from the pontine-medullary junction.
CN 7 - Facial Nerve: controls muscles of facial expression and conveys taste sensations from 2/3 of the tongue and oral cavity.
CN 8 - Vestibulocochlear nerve: responsible for balance and hearing. Arises most laterally from pontine-medullary junction.

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10
Q

What cranial nerves arise from the medulla, and what are their function(s)?

A

CN 9: Glossopharyngeal Nerve: receives sensory and taste fibres as well as supplying parasympathetic to a large area.
CN 10 - Vagus Nerve: supplies parasympathetic fibres to ALL the organs, except adrenal glands, below neck and down to the transverse colon.
CN 11: Accessory nerve: controls the sternocleidomastoid and trapezius muscle arising from the inferior part of the medulla.
CN 12: Hypoglossal Nerve: innervates muscles of the tongue.

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11
Q

What are the types of nuclei and their locations for cranial nerves 3-4?

A

CN III: Oculomotor nucleus is GSE from midbrain. Eidinger-Westphal nucleus is GVE from midbrain.
CN IV: Trochlear nucleus is GSE from midbrain.

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12
Q

What are the types of nuclei and their locations for cranial nerves 5-7?

A

CN V: Trigeminal nucleus is GSA from midbrain-cervical spinal chord. V3 trigeminal nucleus is SVE from pons.
CN VI: Abducens nucleus is GSE from pons.
CN VII: Solitarius nucleus is GVA/SVA in medulla and Salivatory is SVE in pons and medulla

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13
Q

What are the types of nuclei and their locations for cranial nerves 8-10?

A

CN VIII: Vestibulocochlear nucleus is SSA from pons-medulla
CN IX: Solitarius nucleus is GVA/SVA in medulla and Ambiguus nucleus SVE in medulla
CN X: Solitarius nucleus is GVA/SVA in medulla and Ambiguus nucleus SVE in medulla and Vagus m nucleus is GVE from medulla.

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14
Q

What are the types of nuclei and their locations for cranial nerves 11-12?

A

CN XI: Accessory nucleus is SVE from cervical spinal chord and Ambiguus nucleus SVE in medulla
CN XII: Hypoglossal nucleus is GSE from the medulla

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15
Q

What are the features of the midbrain?

A

Looks like upside-down mickey mouse. The ‘ears’ are the cerebral peduncles (crux cerebri).
The oculomotor server arises from the interpeduncular fossa.
Aqueduct shows you’re looking at the midbrain. Around the aqueduct are the inferior colliculi and substantia nigra.

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16
Q

Why is the substantia nigra black?

A

They are filled with neuromelanin which is a byproduct of dopamine metabolism. The older one is, the more they have accumulated (except in Parkinsons disease).

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17
Q

What are the features of the pons?

A

Distinguishing features include the transverse fibres, which run between the two middle cerebellar peduncles.
The fourth ventricle is another clue that you’re at the pons. The trigeminal nerve mergers laterally from the pons.

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18
Q

What are the features of the medulla?

A

The inferior olivary nucleus is very important in motor function. The structure is unique to the upper medulla. There is also the remergence of the corticospinal tract in the form of pyramids. There is still the fourth ventricle in the upper medulla.
The dorsal columns and central canal are visible in the lower medulla.

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19
Q

What are the symptoms of Lateral medullary syndrome (arrises due to thrombosis of the vertebral artery) ?

A
  • Vertigo (damage to the vestibular nucleus)
  • Ipsilateral cerebellar ataxia (one sided shuffle) due to damage from the inferior cerebellar peduncles.
  • Ipsilateral loss of pain/thermal sense in the face (damage to the trigeminal spinal nucleus)
  • Signs of Horners syndrome (ptosis, miosis, lack of sweating)
  • hoarseness (damage to nucleus ambiguus)
  • difficulty in swallowing
  • contralateral loss of pain/thermal sense in trunk and limbs due to damage of spinothalamic tract
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20
Q

How is the Neural tube formed?

A

The neural tube forms from the germinal layers (Ectoderm, Mesoderm, and Endoderm). A strip of he ectoderm thickens and becomes the neural plate. The proliferation of the neural plate forms a neural fold, which eventually fuses at the midline to form the neural canal. Not all of the cells of the neural tube wall fuse, but form a separate source of neural tissueL the neural crest.

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21
Q

Where is the distinction made between the CNS and PNS during the development of the nervous system?

A

The neural tube forms the cells of the CNS, while the neural crest forms the PNS.

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22
Q

What cells do the neuroepithelium of the neural tube and neural crest differentiate into?

A

Neural tube: Neuroblasts forms all neurones with cell bodies in the CNS. Glioblasts develop into neuroglia such as astrocytes and oligodendrocytes. Ependymal cells are cells that line the ventricles and central canal.

Neural crest cells differente into: sensory neurones of the dorsal root ganglia and cranial ganglia; Post-Ganglionic autonomic neurones; schwann cells; non-neurone derivatives.

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23
Q

Explain how the cells from the neural crest differentiate into layers.

A

A cell ready to undergo mitosis contracts towards the inner membrane of the neuroepithelium. One of the daughter cells remains attached to this inner membrane, and eventually returns to the cell cycle, proliferating. The other daughter cell migrates and begins to differentiate. If the cell is a neuroblast, it grows processes and are then directed away from the cell. Early stages of grey and white matter differentiation.

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24
Q

Explain the development of the spinal chord

A

There are three layers (ependymal, grey and white) of the developing spinal chord.
The grey matter divides into two plates dorsally (alar) and two plates ventrally (basal plates).
- The neuroblasts in the alar plates develop into interneurones with sensory function
- The neurones in the basal plate also develops into interneurones, but also motor neurones that send their axons out via ventral rout to peripheral nerves.

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25
Q

How is the development of the spinal chord influenced?

A

Dorso-ventral patterning occurs due to signalling molecules. Those produced by the notorchord influence the cell to become a motor neurone (thus the formation of the basal plate). The ectoderm also produces signals to prevent motor neurone function production. Due to concentration gradients, this forms an alar plate.

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26
Q

Describe the development of the brain by week 4

A

The brain develops from the most anterior tip of the neural tube. Differential growth of the neural tube gives rise to three bulges called primary vesicles. This is the prosencephalon (future forebrain), mesencephalon (future midbrain) and rhombocephalon (future hindbrain).

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27
Q

Describe the development of the brain from week 4 to week 5

A

The three primary vesicles give rise to 5 secondary vesicles. The forebrain divides into the telencephalon and diencephalon. The mesencephalon (midbrain) remains, and the rhombocephalon divides into the pons and medulla.

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28
Q

Describe the development of the brain from week 5 to week 8

A

Further development and reduction of the internal space (forming the ventricular system). There are two lateral vesicles in the developing hemispheres, the third vesicle bisects the diencephalon. The aqueduct goes through the midbrain, and the fourth ventricle is in the hindbrain.

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29
Q

What folds do the primary vesicles make during brain development?

A

Flexures known as the cephalic, pontine and cervical flexures between the prosencephalon, mesencephalon and rhombocephalon respectively.

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30
Q

Why are the sensory nuclei more lateral than the motor nuclei in the developing brainstem?

A

The brainstem has a similar structure to the spinal chord except that the fourth ventricle opens up in the brainstem. This means that the alar plates are more lateral to the basal plates than dorsal to them.

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31
Q

Describe the development of the cortex

A

There is a layer of grey matter cortex over the while cerebral hemispheres. To get the grey matter cells there, they have to undergo a large amount of migration from the germinal later. To do this, cells attach themselves to the process of special radial glial cells. Cells move up towards the hemispheres in waves of proliferation. This continues until there is the typical six-layered structure of the cortex. The timing of this migration and proliferation is very important.

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32
Q

What are the main causes of spinal chord injuries?

A

Traffic accidents, fall and sports. They tend to occur in men more frequently than in females, with the cervical cord often affected.

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33
Q

Why would damage to the white matter of the spinal chord be more devastating than the grey matter?

A

Grey matter consists of cell bodies of interneurones and motor neurones. Damage may affect a few motor neurones, and may not be disastrous.
White matter contains interneurones and ascending/descending tracts. Damage is likely to have severe consequences as function below legion will also be impaired.

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34
Q

Why does the spinal chord contain 31 nerves?

A

All spinal nerves, except the first, exit below their corresponding vertebrae. In the cervical segments, there are 7 cervical vertebrae and 8 cervical nerves . C1-C7 nerves exit above their vertebrae whereas the C8 nerve exits below the C7 vertebra. Therefore, each subsequent nerve leaves the cord below the corresponding vertebra. This means there are 8 cervical nerves, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal (although coccyx is made of 3-4 fused vertebrae).

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35
Q

What types of neurones are associated with dorsal roots and ventral roots?

A

Dorsal roots contain axons of sensory neurones. Ventral roots contain the axons of motor neurones.

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36
Q

Where does the spinal chord end?

A

L2 at the conus medularis.

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37
Q

How is the lower end of the spinal chord anchored to the coccygeal vertebrae?

A

By a pial thread called the filum terminale.

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38
Q

What is below the end of the spinal chord?

A

The lumbar cistern, containing the lumbar and sacral spinal chord (chorda equina)

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39
Q

Describe the two enlargements of the spinal chord

A

The cervical enlargement corresponds roughly to the brachial plexus, which includes spinal segments C5-T1. The lumbosacral enlargement corresponds to the lumbosacral plexus nerves, comprises of segments L2 to S3, and is found about the vertebral levels of T9 to T12.

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40
Q

What is likely to occur in sacral chord damage?

A

Loss of bladder and bowel function - can be due to spina bifida.

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41
Q

What is likely to occur in thoracic chord damage?

A

Loss of lower limb function as well as incontinence (paraplegia)

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42
Q

What is likely to occur in cervical chord damage?

A

Loss of upper and lower limb function and incontinence (quadriplegia)

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43
Q

What is likely to occur due to a lesion high up in the spinal chord (C1/C2)?

A

Cannot breathe unassisted, as the phrenic nucleus controls the diaphragm (innervated by C3, C4 and C5)

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44
Q

Describe the meninges of the spinal chord

A

Three layers of the meninges including dura mater, arachnoid mater and pia mater. CSF flows between pia mater and arachnoid mater (subarachnoid space). Spinal meninges have an extradural space containing a fat and venous plexus. The pia mater also has lateral projections called denticulate ligaments which extend to the dura mater and help stabilise the spinal.

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45
Q

What three spinal chord tracts are the most important with regards to spinal chord injury?

A

Dorsal columns pathway, spinothalamic pathway and lateral corticospinal pathway.

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46
Q

What information is carried by the dorsal columns pathway?

A

Touch, proprioception and vibration

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47
Q

What information is carried by the spinothalamic tract?

A

Pain and temperature

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48
Q

What are the two main pathways of the dorsal columns, and when are they used?

A

If primary axon enters below T6, it will travel up the fasciculus gracilis; if primary axon enters above T6, it travels in the fasciculus cutaneous (more medial).

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49
Q

Describe the pathway of touch, proprioception and vibration information.

A

If primary axon enters below T6, it will travel up the fasciculus gracilis; if primary axon enters above T6, it travels in the fasciculus cuneatus (more lateral) of the DORSAL COLUMNS.
The primary axons synapse with a secondary neurone at the medulla forming the internal arcuate fibres. These fibres decussate at the lemniscus, and continue ascending on the contralateral side forming a pathway called the medial lemniscus.
The secondary axons terminate at the ventral posterolateral nucleus (VPL) of the thalamus, where they synapse with tertiary neurones.
The tertiary neurones ascend via the posterior limb of the internal capsule, ending at the primary sensory cortex.

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50
Q

Describe the pathway of pain and temperature information.

A

In the SPINOTHALAMIC pathway, primary neurones enter the spinal chord, and then ascend one or two levels before synapsing in the substantia gelatinosa with secondary neurones. The primary neurone tract is called Lissaeur’s tract.
The secondary axons decussate and ascend in the anterior lateral portion of the spinal chord. The tracts ascend all the way to the VPL of the thalamus, where it synapses with tertiary neurones. These then ascend via the posterior limb of the internal capsule to the primary sensory cortex.

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51
Q

Where do the two main sensory tracts decussate?

A

Dorsal column pathway decussates in the medulla (at the lemniscus); Spinothalamic pathway decussates a few levels superiorly to where the primary axon enters the spinal chord (much lower down).

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52
Q

What is the degree of the deficit following a spinal chord injury determined by?

A

1) loss of neural tissue
2) vertical level of lesion
3) transverse plane (which tracts are affected)

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53
Q

What is synringomyelia?

A

A disorder in which a cyst or cavity forms within the spinal chord.

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54
Q

How much oxygen, cardiac output and liver glucose does the brain use?

A

20% of O2 consumption, 10-20% of cardiac output and 66% of liver glucose.

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55
Q

What are the two main sources of blood to the brain?

A

The vertebral arteries, which join to make the Basilar artery; and the internal carotid arteries.

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56
Q

Describe the Circle of Willis

A

The Basilar artery splits into the Posterior cerebral arteries. The posterior communicating arteries join this to the middle cerebral artery, which is continuous with the internal carotid. From the middle cerebral artery comes the anterior cerebral artery. The anterior communicating artery connects the two anterior cerebral arteries.

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57
Q

Where does the common carotid artery split?

A

It bifurcates at about the level of the laryngeal prominence, into internal and external common carotid.

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58
Q

How do the vertebral arteries enter the skull?

A

Through the transverse foramina at the base of the skull.

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59
Q

Describe the venous drainage of the brain

A

Cerebellar veins drain into the venous sinuses. The venous blood circulates to the back of the head, and moves naturally through the lateral sinus and sigmoidal sinus to become continuous with the internal jugular vein.

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60
Q

Define stroke

A

A stroke is a cerebrovascular accident; a rapidly developing focal disturbance of brain function of presumes vascular origin which lasts for more than 24 hours.

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61
Q

What are the two main causes of a stroke?

A

Due to an infarction (85%) or haemorrhage (15%).

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62
Q

Define Transient Ischaemic Attack

A

A rapidly developing focal disturbance of brain function of presumed vascular origin that completely resolves within 24 hours.

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63
Q

Define infarction

A

The degenerative changes which occur in tissue following occlusion of an artery.

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64
Q

Define Cerebral Ischaemia

A

The lack of sufficient blood flow to nervous tissue resulting in permanent damage if blood flow is not restored quickly.

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65
Q

How many deaths are as a result of stroke un the UK?

A

100,000 annually - 3rd commonest cause of death.

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66
Q

What results from occlusion of an anterior cerebral artery?

A

Paralysis of the contralateral leg more commonly than arm, and also the face. Frontal lobe function is affected, hence disturbance of intellect, judgement and executive function.

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67
Q

What results from occlusion of a middle cerebral artery?

A

‘classic stroke’ presenting with contralateral hemiplegia in the arm more often than leg, contralateral hemisensory deficits, hemianopia and aphasia.

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68
Q

What results from occlusion of a posterior cerebral artery?

A

Visual deficits, like homonymous hemianopia. Receptive aphasia.

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69
Q

What is a lacunar infarct?

A

A stroke of a penetrating artery providing blood to the brain’s deep structures. Usually associated with hypertension.

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70
Q

What is a heamorragic stroke?

A

An artery supplying the brain (not meninges) ruptures leading to disturbance of brain function.

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71
Q

In general, what causes the different haemorrhages between the meninges?

A
Epidural haemorrhage (artery ruptures between skull and dura) usually due to trauma.
Subdural haemorrhage (vein ruptures between dura mater and brain) usually due to shearing forces.
Subarachoind haemorrhage (blood vessel ruptures between arachnoid mater and pia mater) usually due to an aneurysm.
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72
Q

What is the good flow rate to the brain?

A

55ml/100g tissue/min (15% of CO)

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73
Q

How does the brain regulate CBF with regards to a change in pressure?

A

A myogenic response. Increased pressure leads to increased stretch of vascular smooth muscle. This causes increased contraction before blood reaches the brain which decreases CBF.

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74
Q

In brief, how can the brain control local blood flow?

A

Neural and Chemical factors

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75
Q

How can the brain control CBF through neural control?

A
  • Sympathetic innervation produces vasoconstriction, but only operates when arterial blood pressure is high
  • Parasympathetic innervation produces slight vasodilation
  • Central cortical neurones release a variety of vasoconstrictor neurotransmitters such as catecholamines.
  • Dopaminergic neurones produce vasoconstriction as they innervate penetrating arterioles and pericytes around capillaries. Pericytes are brain macrophages with diverse function, and can be found associated with capillaries.
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76
Q

How can the brain control CBF through chemical control?

A

Metabolically active cells release factors and effect surroundings. CO2, pH, NO, K+, adenosine and anoxia are vasodilatory factors.

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77
Q

What are circumventricular organs?

A

Those that lie outside the blood-brain barrier.

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78
Q

How much CSF is there?

A

80-150 ml

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79
Q

How is the CSF made?

A

Choroid plexus secretes CSF into the lateral ventricles.

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80
Q

How is the Blood-Brain Barrier maintained?

A

It consists of endothelial cells with tight junctions. Capillaries are also non-fenestrated and surrounded by astrocyte end-feet.

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81
Q

Give examples of circumventricular organs

A

Median eminence of hypothalamus
Subfornican organ
Organum vasculosum of the lamina terminalis

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82
Q

Describe the difference between plasma and CSF

A

Total osmolarity is the same. Important difference between specific molecules e.g CSF has less calcium. This means that the pH of the fluids are slightly different, with the CSF being slightly more acidic.

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83
Q

What is the diencephalon?

A

The compartment of the forebrain that contains the thalamus and hypothalamus.

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84
Q

How is the thalamus divided between the hemispheres?

A

Although the thalamus exists in two halves, the separate nuclei in each half communicate with each other. It has ipsilateral connection with the forebrain.

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85
Q

What is the thalamus not involved in?

A

Olfaction

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86
Q

How is the thalamus split?

A

EACH thalamus is divided into two halves: smaller posterior half, larger anterior half.

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87
Q

What are the categories of thalamic nuclei?

A

Specific nuclei: connect with the primary cortical areas
Association nuclei: have more diffuse connections with the association cortex
Intralaminar nuclei: are nuclei which are embedded in the lamina dividing the thalamus

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88
Q

What are the specific thalamic nuclei and their functions?

A
  • Ventral Lateral Nucleus: connected with the motor cortices for co-ordination and planning
  • Ventral Anterior Nucleus: connected with the motor cortices for planning and inhibition of unwanted movement
  • Ventral Posterolateral Nucleus: connected with primary somatosensory cortex for touch and proprioception information about the body
  • Ventral Posteromedial Nucleus: connected with primary somatosensory cortex for touch and proprioception information about the brain
  • Lateral geniculate nucleus: connected with visual system sending information to primary visual cortex
  • Medial geniculate nucleus: connected with the auditory nucleus, acting as a relay between inferior colliculus and primary auditory cortex.
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89
Q

What are the association thalamic nuclei and their functions?

A
  • The anterior, lateral dorsal, and dorsomedial nuclei connect with part of the limbic system (cingulate and prefrontal cortex)
    The lateral posterior, and pulvinar nuclei connect with the association cortex at the parieto-temporo-occipital junction and the prefrontal cortex.
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90
Q

What are the functions of the intralaminar nuclei?

A
  • They form part of the reticular activating system; responsible for the control of the level of arousal of the brain by modulating the level of activity of the cerebral cortex
  • They receive input from the reticular formation of the brainstem, and then project diffusely throughout the cortex
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91
Q

What is the reticular nucleus?

A

It is a fine sheet of neurotissue lying over the lateral surface of the thalamus like a net, giving good access to the thalamic nuclei, but does not have any direct connections with the cortex itself. It receives input from the reticular formation of the brainstem (therefore a part of the RAS) and indirectly regulates the flow of information within the reticular activating system to the cortex.

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92
Q

How does thalamic syndrome present?

A

Results in contralateral hemianaesthesia, followed by burning pain often accompanied by mood swings.

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93
Q

Where does the hypothalamus lie?

A

Inferior and anterior to the thalamus, posterior to the optic chasm and pituitary infundibulum.

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94
Q

What hypothalamic neurones project into the posterior pituitary?

A

Paraventricular and Supraoptic neurones that contain oxytocin and vasopressin.

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95
Q

Through what systems does the hypothalamus control homeostatic mechanisms?

A
  • autonomic nervous system
  • endocrine system
  • controlling behaviour
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96
Q

What forebrain structures are associated with the hypothalamus?

A

The olfactory system and limbic system.

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97
Q

What behaviours does the hypothalamus control?

A
  • eating and drinking via appetite sensors
  • expression of emotion
  • sexual behaviour
  • circadian rhythm
  • memory
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98
Q

How will a patient with a hypothalamic tumour present?

A

Polydipsia and polyuria; Amennorhea. Later present with liable emotions, rage, inappropriate sexual behaviour, memory loss, hyperphagia. Temperature fluctuations; decreased thyroid function; decreased adrenal cortex and gonadal function

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99
Q

Define proprioception

A

The ability to determine the positioning of joints and the length of muscle to appreciate the body’s organisation in space.

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100
Q

What type of receptors detect sensory information?

A

Touch and proprioception are realised by mechanoreceptors. Temperatures by thermoreceptors, and pain by nociceptors.

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101
Q

What are the different types of mechanoreceptors?

A

Plexuses are naked nerve endings on skin
Peritirichal endings are those wrapped around hair follicles
Merkel ending in epidermis
Pacinian corpuscules is suited to detecting vibration as it around a group of cells
End bulb
Meissiner’s corpuscles
Ruffini endings

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102
Q

What determines the function of the mechanoreceptors?

A
  1. degree of specialisation
  2. location
  3. physiological properties
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103
Q

What parameters of mechanoreceptors can be modified?

A
  • activation threshold, which determines sensitivity
  • slow or fast adapting. Slow adapting is where APs are produced from when stimulus starts to until it ends. Fast adapting produce APs as soon as the stimulus starts but stops quickly afterwards, some may have a burst of firing when stimulus stops.
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104
Q

Where are slow and fast adapting mechanoreceptors found?

A

Slow adapting are found in systems where the parameter needs to be constantly monitored e.g joints and muscles
Fast adapting are used for monitoring stimulus that move or change quickly and that that persist but do not require monitoring.

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105
Q

What is the receptive field of a receptor?

A

The area that can trigger the sensory neurone. The larger the receptive field, the lower the acuity. Density varies over the body and receptive fields overlap. There are smaller and more receptive fields in the fingertip than trunk.

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106
Q

How is the intensity of a stimulus coded?

A

The frequency of firing of the neurones, related to a logarithmic scale.

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107
Q

What is lateral inhibition of neurones?

A

The capacity of an exited neurone to reduce the activity of its neighbours. This sharpens the spacial profile of excitation in response to a localised stimulus. Only neurones which are most stimulated and least inhibited will fire

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108
Q

How can AXONS be classified?

A

An alphabetical system refers to neurones based on diameter. A is largest diameter.
The roman numeral system classifies by conduction velocity. 1 is fastest.
The two systems correlate.

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109
Q

How does sensory information of touch, proprioception and vibration of the face and head reach the cortex?

A

Sensory information comes from the trigeminal nerve, which synapses with secondary neurones in the PONS, where they decussate and join with the other axons from the dorsal columns at the medial lemniscus.

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110
Q

Explain the cortical analysis of touch, proprioception information.

A

Somatosensory cortex has a somatotrophic arrangement known as the homunculus. Information arrives into the S1 area of the somatosensory cortex where it is analysed before being further analysed at the S2 area/

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111
Q

Where is the somatosensory cortex?

A

It is located in the postcentral gyrus which is just posterior to the central sulcus.

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112
Q

What are the parts of the cerebral motor cortex?

A

Primary Motor Cortex / M1 / Broadmann’s area 4
Premotor Cortex / Broadmann’s area 6
Supplementary Motor Area / Broadmann’s area 6

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113
Q

Where is the primary motor cortex located?

A

On the frontal lobe, on the pre central gyrus just anterior to the central sulcus.

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114
Q

Describe the organisation of motor neurones in the cortex

A

Homunculus layout

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115
Q

How are the different areas of the motor cortex connected?

A

The premotor cortex and supplementary motor area have reciprocal connection, and both independently provide reciprocal connections to M1.

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116
Q

What’s the function of the supplementary motor area?

A

It is involved in planning internally driven voluntary movements. It involves many muscle groups, rather than highly specific movements.

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117
Q

What’s the function of the premotor area?

A

Premotor area is necessary to prepare M1 for the motor act. Especially involved in planning externally driven movement such as reacting to visual cues.

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118
Q

What would result from a lesion in the:

a) Supplementary Motor Area
b) Premotor Area

A

a) Lack of spontaneous movements and speech

b) Slow complex movements as M1 neurones take longer to get into actions without sufficient facilitations from PMA.

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119
Q

What are the stages of motor control?

A

1) Strategy - planning of movements requires somatosensory cortex, prefrontal cortex and motor association cortices. It also involves feedback information via the basal ganglia and thalamus.
2) Tactics - identify sequence of muscles to execute movement, involves primary motor cortex with feedback from cerebellum and thalamus
3) Execution - requires activation of motor neurone pools as well as spinal chord and brainstem.

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120
Q

What are the descending motor pathways?

A

The Corticospinal (Pyramidal) tract:

  • Lateral corticospinal tract
  • Anterior corticospinal tract

The Subcorticospinal (Extrapyramidal) tract:

  • Rubrospinal tract
  • Reticulospinal tract
  • Vestibulospinal tract
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121
Q

Describe the pathway of the corticospinal tract

A

Originates from pyramidal cells in LAYER V of the primary motor cortex, integrating inputs from the somatosensory cortex.
Axons protect through the cerebral white matter and into the POSTERIOR LIMB of the Internal Capsule where they continue down into the brainstem.
Fibres travel via CEREBRAL PEDUNCLES in the medulla where they form column-like structures called pyramids.
At the medulla 80% decussate to form the lateral corticospinal tract, while 20% remain uncrossed to form the anterior corticospinal tract.
Axons project into the ventral horns, where they connect with the lower motor neurones, which provide innervation for voluntary muscles.

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122
Q

What information is carried by the corticospinal tract?

A

Information for voluntary, fine movements - mainly for the arms and legs.

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123
Q

What information is carried by the subcorticospinal tract?

A

Supporting voluntary movement (still beyond voluntary control), controlling axial muscles, helping to control posture, and locomotion in automatic movements. They receive substantial input from the basal ganglia, cerebellum and BRAINSTEM NUCLEI.

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124
Q

Describe the rubrospinal tract

A

It passes through the superior cerebellar peduncles to the RED NUCLEUS in the midbrain, and finally to the spinal nerves, carrying information important for muscle tone and posture.

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125
Q

Describe the vestibulospinal tract

A

Runs from the VESTIBULAR NUCLEI located in the lower pons and medulla, to the spinal nerves, carrying information about balance.

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126
Q

Describe the reticulospinal tract

A

Runs from the RETICULAR NUCLEI of the pons and medulla to the spinal nerves, carrying information about somatic motor control and autonomic functions.

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127
Q

What do we call the disease caused an upper motor neurone lesion before, during or shortly after birth?

A

Cerebral palsy

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128
Q

What are lower motor neurones

A

A nerve cell that goes from the spinal cord to a muscle. All spinal nerves have a lower motor neurone component as they are mixed nerves. Only some cranial nerves have a lower motor neurone component.

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129
Q

What are the signs and symptoms of an Upper Motor Neurone Lesion?

A

1) Weakness
2) Spasticity - increased tone in affected muscles
3) Hyperrelexia - increased muscle stretch reflexes
4) Babinski sign - Abnormal plantar reflex where scratching lateral margin of foot from heel towards toe causes plantar extension as opposed to normal plantar flexion.

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130
Q

What are the signs and symptoms of an Lower Motor Neurone Lesion?

A

1) Weakness
2) Muscle Wasting
3) Tongue fasciculations
4) Nasal speech
5) Dysphagia
6) Hyporeflexia
7) Fibrillations

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131
Q

By what receptors is pain realised by?

A

Nociceptors

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132
Q

By what spinal chord tract does pain information travel through?

A
  • Visceral pain by spinothalamic AND dorsal columns

- Somatic pain by spinothalamic

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133
Q

What are the properties of nociceptors?

A
  • Polymodal (can respond to a variety of stimuli)
  • Free nerve endings
  • High threshold (compared to touch receptors)
  • Slow adapting
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134
Q

What axon types can nociceptors have?

A
  • A(delta) (group III) is a mechano or thermoreceptor produces sharp pain
  • C fibres (group IV) are chemoreceptors (bradykinin and histamine) produces dull aching pain
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135
Q

To what destinations does the spinothalamic tract carry pain information to?

A
  • VPL and VPM nucleus of the Thalamus –> S1 and S2 cortex
  • Brainstem for perception of pain
  • Periaqueductal Grey area of the midbrain to inhibit pain
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136
Q

Describe the spinothalamic pathway

A

Primary neurones synapse with secondary neurones straight away in the dorsal horn. The secondary neurones decussate at the spinal chord. As neurones enter the spinal chord as you travel up, they are added in a specific somatotropin organisation. More axons added medially. Axons synapse with tertiary neurones in the VPL nucleus in the thalamus.

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137
Q

How does pain stimuli from the face reach the thalamus?

A

Carried by the trigeminal nerve (fibres from trigeminal nucleus in the medulla). The axon continues down in the medulla until it reaches the trigeminal nucleus, where it synapses with a secondary nucleus which decussates and joins the spinothalamic tract. It then joins the VPM nucleus of the thalamus.

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138
Q

How is pain perceived in the brain?

A

The thalamus sends information of pain to the appropriate part of S1, which localises and realises the intensity of the stimulus. Pain sensation is perceived by sub-cortical areas:

  • collateral branches from the spinothalamic tract reaches the reticular formation to increase awareness of stimuli
  • other branches reach intralaminar nuclei, hypothalamus, forebrain and limbic system to modulate mood, emotion and motivation.
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139
Q

State the two ways pain perception is dampened down

A
  • Peripheral local inhibition

- Central descending inhibition

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140
Q

Describe how peripheral local inhibition works

A

This occurs in the dorsal horn. Before a primary nociceptive neurone synapses with a secondary neurone in the dorsal root it ALSO synapses with an interneurone. A mechanoreceptor also synapses with this neurone. The mechanoreceptor will send excitatory signals to the interneurone, which synapses with the same secondary neurone of the spinothamic tract sending inhibitory signals. The primary nociceptive neurone sends inhibitory signals to this interneurone.

This results in a dampening down of pain sensation when mechanoreceptors are also activated. This is why rubbing a itchy or painful area reduces pain sensation.

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141
Q

Describe how central descending inhibition works

A

This is caused by a group of neurones surrounding the aqueduct in the midbrain - the periaqueductal grey matter. If their stimulation is sufficient from the rest of the brain, they feed impulses down the reticular formation of the medulla into the dorsal horn.
There they synapse with secondary projection neurones entering the spinothalamic pathway inhibiting them.

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142
Q

What disorders result in nociceptive dysfunction?

A
  • Syringomyelia is damage in the cerival region which disrupts fibres from crossing over. Patients present with cuts and bruises on hands due to loss of nociception
  • Charcot joints is a hereditary condition caused by a lack of development of nociceptors, resulting in a loss of joint pain, leading to overuse and inflammation
  • Wind-up dorsal horn happens when chronic stimulation leads to lowered pain threshold and continuous sensation despite removal of noxious stimuli
  • Thalamic syndrome is a disorder there is damage to the thalamus, leading to pain hypersensitivity, and poorly localised central pain that doesn’t respond to local pain killers
  • Psychological (neuropathic pain) is where the physical stimulus cannot be found.
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143
Q

What are the components of the Basal Ganglia?

A
  • Caudate and putamen
  • Internal (medial) and external (lateral) part of Globus Pallidus
  • Subthalamic nucleus
  • Pars reticulata and Pars compacta of the substantia nigra in the midbrain.
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144
Q

How do thoughts from the frontal cortex get converted into motor activity?

A

Cortex -> Striatum -> Globus Pallidus -> VL nucleus of Thalamus -> Supplementary Cortex Area

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145
Q

Describe the basal ganglia motor loop

A

Axons from cerebral cortex -> Putamen and Caudate nucleus.
From putamen there are two pathways:
1) Direct: -> Globus Pallidus internal and Substancia Nigra pars reticulata
2) Indirect: Globus Palidus external -> Subthalamic nuclei -> internal
There are then outputs from the Globus pallidus internal and Substancia Nigra pars reticulate to the THALAMUS (-> motor cortices)
The GPi and SNr INHIBIT the thalamus (and thus motor cortex). The putamen inhibits the GPi which in turn releases the thalamus from inhibition.

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146
Q

What is the nigro-striatal pathway?

A

Input (excitatory) to the putamen or caudate nuclus from substancia nigra pars compacta

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147
Q

Describe the pathophysiology of Parkinson’s disease

A

Neuronal degradation of the substania nigra means reduced dopamine in the striatum (less excitation) -> decreased inhibition of the globus pallidus -> increased inhibitory output to the thalamus -> decreased fasciculations of the motor cortex.

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148
Q

What are the signs of Parkinson’s disease?

A

Bradykinesia, Hypomimic face, Akinesia (difficulty in initiating movements), Rigidity, Tremor at rest, Parkinson’s gait.

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149
Q

Describe the pathophysiology of Huntington’s disease

A

huntingtin gene on chromosome 4 defect leads to degradation of the inhibitory pathway neurones (GABAergic) in the straitum, selective to the indirect pathway. Less inhibitory output to the thalamus -> thalamic neurones firing randomly and inappropriately -> chorea

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150
Q

How can the cerebellum be split anatomically?

A
  • two hemispheres separated by a vermis

- three lobes horizontally: anterior, posterior and floculonodular lobes

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151
Q

How is the cerebellar cortex organised?

A

The cerebellum is a highly folded layer of grey matter, underneath which exists myelinated nerve fibres and cerebellar nuclei. The cortex itself can divided into three layers:

  1. Molecular layer (top)
  2. Purkinje cells
  3. Granular cell layer
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152
Q

Describe the two types of fibres of the inputs into the cerebellar cortex

A

1) Moss fibres enter at granular layer from pontine nuclei and synapse with the purkinje cells
2) Climbing fibres enter at the Purkinje cell layer and originate from the contralateral inferior olive (medulla)

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153
Q

What are the outputs of the cerebellum and what information do they carry?

A

1) Fibres from dentate nuclei - motor planning and voluntary movements - projections to thalamus and red nucleus
2) Fastigal - involved in balance, has projections to the vestibular and reticular nuclei
3) Interposed - also involved in balance, but projections to the thalamus and red nuclei.

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154
Q

What are the three sources of input into the cerebellum, and through what peduncle do they enter the cerebellum?

A

1) Mossy fibres from the spinocerebellar pathway (proprioceptive info) go through the inferior cerebellar peduncle.
2) Climbing fibres from the inferior olive go through the inferior cellebelar peduncle
3) Mossy fibres from the pons bringing information from cerebellar cortex enter through middle cerebellar peduncle.

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155
Q

What are the functional divisions of the cerebellum?

A

Vestibulocerebellum, Spinocerebellum and Cerebrocerebellum

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156
Q

Describe the function of the Vestibulocerebellum

A

Lives in the flocculonodular lobe, and has inputs and outputs to the vestibular nuclei and vestibular nerve via the inferior peduncle.

  • Regulation of gait, posture and equilibrium
  • Coordination of head movements with eye movements. (vestibulo-oculo reflex)
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157
Q

Describe the function of the Spinocerebellum

A

Is the vermis and adjacent strips. Contains the fastigal and interposed nuclei. Spinal afferent tracts from axial portions of the body, trigeminal, visual and auditory inputs project into vermis. Spinal afferents from the limbs project into the immediate nuclei.

  • Speech co-ordination
  • Adjustments of muscle tone and coordination of limb movements
158
Q

Describe the function of the Cerebrocerebellum

A

The lateral lobe contains the dentate nucleus.

  • Co-ordination of skilled movements, tactics of skilled movements
  • Cognitive function, attention, language and emotional processing
159
Q

What are the main signs of cerebellar disorders?

A

VESTC: Ataxia, Romberg sign (instability when eyes are closed), and Nystagmus (involuntary eye movement)
SPINOC: Hypotonia, Dysarthria (slurred speech)
CEREBROC: Dysmetria (inappropriate force and distance for target-directed movements), Dysdiadochokinesia (inability to coordinate movements and inability to perform rapid alternating movements)
GENERAL: Intention tumour, scanning speeches

160
Q

What are motor neurone diseases?

A

MND is a group of neurological disorders that selectively affect motor neurones causing progressive weakness of many neurones. It affects upper and lower motor neurones.

161
Q

What is the most common cause of motor neurone disease?

A

Most causes are sporadic. However, familial MND accounts for about 10% of cases.

162
Q

What are the early symptoms of motor neurone diseases?

A
  • Stumbling due to leg muscles
  • Difficulty holding objects due to weakness
  • Slurring speech or swallowing difficulties
  • Cramps and muscle twitching (fascinations)
163
Q

What is ALS?

A

Amyotrophic Lateral Sclerosis is the degeneration of the corticospinal tract and chromatolysis with associated disconnection of neurones from target muscles fibres. Staining reveals mosaic patterns with decrease in myosin ATP and muscle atrophy is observed.

164
Q

What are the two types of potentials that can be initiated by synaptic transmission?

A
  • excitatory post-synaptic potential (EPSP) is when the cell membrane is made less negative and this closer to the threshold potential
  • inhibitory post-synaptic potential (IPSP) is when the cell membrane is made more negative, making it closer to the threshold potential
165
Q

What are the types of synaptic summation?

A

Temporal summation is when an action potential is achieved due to increased frequency of impulses
Spatial summation is where an action potential is achieved due to input from multiple presynaptic cells

166
Q

What is a neuromuscular junction?

A

The NMJ is a specialised synapse between the motor neurone and the motor end plate (muscle fibre cell membrane)

167
Q

Describe the transmittance of an action potential through a NMJ

A

The AP arrives at the pre-synaptic bouton, causing Ca2+ channels to open leading to Ca2+ before ACh release into the cleft.
Specialised foldings of the muscle fibre membrane will pick up the ACh and act on receptors
ACh binds to nicotinic acetylcholine receptors, causing ion channels to open, allowing Na+ influx

168
Q

Describe the activity at the NMJ at rest and during an AP

A

At rest, miniature packets of ACh are released into the synapse causing minute end-plate potentials (MEPPs), which are not powerful enough to cause an AP.
Arrival of the AP triggers the release pf 200-300 quanta, producing numerous MEPPs, which sum to produce a depolarisation to -20mV (endplate potential)

169
Q

What is a lower motor neurone?

A

A lower motor neurone is a motor neurone whose cell body lies in the ventral horn of the spinal chord or cranial nerve nuclei and that directly innervates the muscle via its axon.

170
Q

What are the types of lower motor neurones?

A
  • alpha-motor neurone (70micrometeres in diameter) innervate the muscle fibres (extrafusial fibres - big mass of muscle) directly to cause constriction
  • gamma-motor neurones (30micrometeres in diameter) innervate the intrafusal fibres (small mass at the centre of the muscle). They have a role in keeping muscle fibres taut but do not adjust lengthening/shortening of muscle, also important in stretch perception.
171
Q

What is a motor pool?

A

All the alpha neurones innervating a single muscle (as opposed to a motor unit)

172
Q

What is a motor unit?

A

A single motor neurone together with all the muscle fibres that it innervates, it is the smallest functional unit that produces force.

173
Q

Why is a muscle fibre only innervated by one motor neurone?

A

During development, lots of motor neurones innervate a single muscle fibre, but one outcompetes the rest.

174
Q

On average (mean), how many muscle fibers are innervated by one motor neurone?

A

600

175
Q

What are the different types of motor units?

A

Type I/Slow: Smallest diamater axons, small dendritic tress, slowest conduction velocity but low fatiguability (60 minutes) therefore used to maintain postural muscles
Type I/Fast: large diameter axons, long dendrtotic trees, fast conduction velocity.
Type IIA are less fatiguable than IIB, and produce moderate tension. Type IIB are more fatiguable (6 mins) and produce high tension.

176
Q

What are the two mechanisms by which the brain can regulate the force a muscle produces?

A

1) Recruitment. Smaller units (Slow/Type1) are recruited first -> Type IIA -> Type IIB. Derecruitment in opposite order. As more force is required, more motor units are recruited allowing for fire control.
2) Rate coding. Motor units can fire at frequencies (generally start at 8Hz) and increase as more force is needed. Summation occurs when units fire at frequency too fast to allow muscle to relax between arriving potentials.

177
Q

What are neurotrophic factors?

A

Type of growth factors which prevent neuronal death, and promote growth of neurones after injury.

178
Q

In what way(s) does a muscle fibre give more than just action potentials to the muscle cell?

A
  • ‘feeds’ it to keep it alive. loss of innervation causes hypertrophy, despite maintaining vasculature.
  • has an effect on its properties, esp regarding if muscle is to be slow or fast twitch.
179
Q

What is a reflex?

A

An automatic and often inborn response to a stimulus that involves a nerve impulse passing inwards from a receptor to a nerve centre and then outwards to an effector without reaching the level of consciousness.

180
Q

What are the components of a reflex?

A
  1. Sensory receptor
  2. Sensory neurone
  3. Integrating centre
  4. Motor neurone
  5. Effector
181
Q

Give an example of a monosynaptic reflex

A

Patella tendon reflex:

1) Stretch sensed muscle spindle, causing AP to travel down sensory neurone
2) It synapses in the spinal chord with the motor neurone required causing the quadriceps to contract
2) It also synapses with an interneurone that causes the antagonist to relax.

182
Q

Give an example of a polysynaptic reflex

A

The flexion withdrawal reflex. It is elicited by noxious stimulation, consisting in flexion on the same side, and extension on the other leg (prevent falling over). The inter-neurones convey information to multiple motor neurones, causing multiple motor units to contract, resulting in effects.

183
Q

Why does upper neurone disease lead to hypereflexia?

A

Higher centers of the CNS exert inhibitory and excitatory regulation upon the stretch reflex - USUALLY INHIBITORY.

184
Q

What is the Jendrassik manoeuvre?

A

If you clench your teeth or make a fist while having the patellar tendon tapped, the reflex is increased!

185
Q

How do humans perceive frequency and amplitude of sound waves?

A

Pitch and loudness respectively

186
Q

What frequencies can the human ear pick up?

A

20-20000 Hz

187
Q

What is the maximum decibels the human ear can hear?

A

120db

188
Q

What is the anatomy of the outer ear?

A

Pinna (auricle), and the auditory CANAL (external acoustic meatus)

189
Q

What is the middle ear composed of?

A

The portion between the tympanic membrane and the oval and round windows: the ossicles (malleus, incus and stapes)

190
Q

What is the inner ear composed of?

A

The cochlea and vestibular apparatus

191
Q

How does the sound wave enter the inner ear?

A

Through the auditory canal –> malleus –> incus –> stapes –> oval window vibrates causing a pressure wave inside the fluid of the cochlea

192
Q

What is the purpose of the middle ear components?

A

Amplify the sounds by 30db

193
Q

How is amplification of sound waves achieved?

A

a) lever system of articulated ossicles

b) a larger area of the tympanic membrane compared to the membrane of the oval window (17:1 ratio)

194
Q

How is the inner ear (stereocillia) protected against too much vibration?

A

1) Reflex contraction of the tensor tympani and strapedius muscle to reduce leverage through the ossicle bridge. Only protects against natural sounds that tend to get gradually louder as contraction of the muscle takes unto 100ms
2) Equilibration of air pressure on either side of the tympanic membrane by the esutachain tube (auditory tube). Eustachian tube connects the middle ear with the back of the nasopharynx behind the nasal cavity.

195
Q

What are the compartments of the cochlea (and what fluid do they contain) ?

A

Scala vestibuli (contains perilymph), Scala media (endolymph) and Scala tympani (perilymph) [from top to bottom]

196
Q

Where are stereo cilia found?

A

On the tips of cochlear hair cells, on the basilar membrane

197
Q

How do pressure waves reach the stereocilia?

A

Sound waves hit the oval window, causing a pressure wave to travel through the scala vestibuli and then the scala tympani. The vibrations travel up and down on the vestibular membrane, causing a pressure wave in the scala media. The pressure wave goes across the basilar membrane (moving stereocilia in the process) and joins the pressure waves in the scalar tympani.

198
Q

What is the organ of corti?

A

The organ of the inner ear that has sensory hair cells. The hair cells are covered by the TECTORIAL membrane with the stereocilia touching it. The tectorial membrane is a gelatinous structure and does NOT vibrate with sound.

199
Q

Why does the scala media have a high K+ concentration>

A

It is lined by the stria vascularis, which maintains a high K+ concentration by secreting endolymph.

200
Q

Describe the innervation of the cochlear hair cells

A

Spiral ganglia from CN VIII (embedded in the modiolus) produces axons that innervates the hair cells. Impulses from the hair cells pass laterally through the modiolus –> vestibulocochlear nerve –> brainstem

201
Q

What are the cells that surround cochlear hair cells called?

A

Support cells

202
Q

How are hair cells connected to the cochlear nerve?

A

The basal membrane of the cell synapses with nerve endings. Movement or deflection of the stereocilia causes depolarisation of the nerve endings.

203
Q

What are the sensory receptor(s) of the auditory, and vestibular systems?

A

Hair cells

204
Q

How are the hair cells in the Organs of Corti arranged?

A

There are inner hair cells and outer hair cells. Arrangement of a single row of inner hair cells followed by 3 rows of outer hair cells.

205
Q

What function do the inner and outer cochlear hair cells do?

A

Inner hair cells provide auditory information. Info from outer hair cells goes to the brainstem and forms a refinement mechanism (adjusting sensitivity)

206
Q

How does movement of the basilar membrane cause depolarisation or not?

A

Movement can be divided into an upwards or downwards phase.
Upwards: movement causes shear forces AWAY form modiolus, moving cilia away. This causes opening of K+ channels and depolarisation of the hair cell.
Downwards: movement causes shear forces directed towards the modiolus causing closure of K+ channels, so no AP is generated.

207
Q

How are stereocilia connected and arranged on the hair cell?

A

Adjacent stereocilia are connected together by tiplinks. Stereocilia are arranged in order of increasing length (away from modiolus)

208
Q

How does movement of stereocilia cause K+ channels to open?

A

During the upwards phase of vibration, there is movement towards the tallest stereocilia, therefore there is greater tension between the tiplinks. The greater distance between the tips causes opening of K+ channels.

209
Q

How sensitive are stereocilia to vibrations?

A

They only need to be deflected 0.3nm (/500nm stereocilia) in order to be detected by the auditory system as a sound.

210
Q

How does the auditory apparatus distinguish between different frequencies of sound?

A

The basilar membrane is a heterogenous structure. Sound will only make part of the membrane that corresponds to the particular frequency to resonate. Lower frequencies cause vibration near the apex, higher frequencies near the base. As the apex membrane is wider and more flexible and base fibres are stiff with narrow membrane.

211
Q

What word can be used to describe the organisation of axons traveling to the auditory cortex?

A

Tonotopic organisation

212
Q

Describe the central auditory pathways

A

Two CN VIII nerves carry impulses to the cochlear nucleus in the medullary-pons junction.
Information is then projected to the superior olive, but also the contralateral superior olive, giving a bilateral projection.
The superior olives then send the impulse to the inferior colliculus before the information is passed to the medial geniculate body in the thalamus. Here the information is processed before it passes into the auditory cortex in the temporal lobe.

213
Q

How is resolution enhanced for similar frequencies of sound?

A

Lateral inhibition of neurones in the central auditory pathway.

214
Q

Describe the parts of the auditory cortex

A

Primary auditory cortex receives auditory input first. It is divided into zones which analyse different frequency ranges. Broadmann areas 41 and 42. Located on the temporal lobe.
The Secondary auditory cortex surrounds the primary auditory cortex and is where neurones respond to more complex sound patterns. Involved in more subtle processes such as quality and tone of sound and musical sound.

215
Q

Define conductive hearing loss

A

Conductive hearing loss is when sound is prevented from reaching the cochlea due to outer or middle ear dysfunction.

216
Q

What are the causes of conductive hearing loss?

A
  • Wax build up
  • Otitis media (middle ear infection –> inflammation –> fluid build up impairing amplification)
  • Otosclerosis of ossicles - bony extensions grow from the ossicles affecting leverage system.
  • Perforated eardrum
  • Congential malformation
217
Q

What are the types of hearing loss?

A
  • Conductive hearing loss

- Sensorineural deficiencies

218
Q

Define sensorineural deficiency

A

These occur when the root cause lies in the vestibulochochlear nerve, inner ear or central processing centers

219
Q

What are the causes of sensorineural hearing loss?

A
  • Presbyacusis - loss of hair cells with ageing
  • Loud noise can cause death to some hair cells
  • Meziere’s disease - drainage problem leading to buildup of pressure affecting hair cells in inner ear.
  • Toxicity (gentomycin can damage hair cells)
  • Acoustic neuroma - benign tumour of CN VIII
  • Viral infections can cause damage to nerves
  • Demyelination in MS
  • Injury to central auditory pathways
220
Q

What parameters can the vestibular system detect, and using what organs?

A

Change in head position and linear acceleration detected by otolith organs.
Angular acceleration is sensed by the semicircular canals

221
Q

Where are the otolith organs?

A

In the utricle and saccule (in the vestibule)

222
Q

Name the epithelium of the otolith organs and their orientation

A

Each otolith organ contains a sensory epithelium called the macula. This is vertical in the sauce, and horizontal in the utricle. Note, the hair cells project at a normal to the plane.

223
Q

Describe the environment of the hair cells in the otolith organs

A

Hair cells lie on the macula (epithelium), among a bed of supporting cells with their cilia projecting onto a gelatinous cap.

224
Q

What directions (of movement) are the cilia of the hair cells sensitive to?

A

Those in the sacule are sensitive to vertical (and antero-postero directions), while those in the utricle are sensitive to horizontal (and antero-postero directions)

225
Q

How is the direction of acceleration realised from outputs of the otolith organs?

A

The vector sum of the urticular and saccule stimulation patters.

226
Q

What are otoliths?

A

They are calcium crystals that sit on the gelatinous cap on top of cilia. When the head accelerates, a force is exerted on the otoliths, which exerts a force in the same direction into the gelatinous cap causing stereocilia to deflect.

227
Q

In what direction do the stereocilia have to deflect in order to lead to hair cell depolarisation?

A

Towards the kinocilium

228
Q

Why are the otolith organs considered to be the static labyrinth?

A

They respond to the static head, its lift and acceleration. When upright, the vestibular ganglion that innervates the saccule has tonic discharge do to constant displacement by gravity.

229
Q

How are the semicircular canals arranged?

A

There are three of them, oriented perpendicular to each other, positioned in three dimensions.

230
Q

Where are the hair cells in the semicircular canal?

A

They are located within sheets of cells called the crista, which are located within a bulge along the canal called the ampulla.

231
Q

Describe the environment of the stereocilia of the semicircular canals

A

They are covered by a jelly-like layer called the capula. The semicircular cabals are filled with endolymph (same as cochlea)

232
Q

How does rotational acceleration translate to depolarisation of semicircular hair cells?

A

Bending of the cilia (towards kinocilium –> depolarisation) is facilitated when rotational acceleration causes the endolymph of the canal to spin, exerting a force to the capula. Like wind on a sail.

233
Q

How do the vestibular apparatuses on opposite ears co-ordinate to sense rotational acceleration?

A

Each canal has a tonic firing rate - the bonuses from both ears balance out. When acceleration cites hair cells on one canal, it inhibits the hair cells on the contralateral canal. This is a ‘push-pull’ arrangement that optimises the brain to detect rotational movements.

234
Q

What are the functions of the vestibular apparatus (otolith organs and semicircular canals)?

A
  • Control balance reactions
  • Provide compensatory reflexes (such as vestibulo-occular reflex)
  • Tune cardio-vascular functions
  • Serve perception of motion in space
  • Provide a spatial reference for other sensory motor co-ordinations
235
Q

To what nuclei does the information from the vestibular system project to?

A

There are four vestibular nuclei (superior, inferior, lateral and medial) for each side.
Otoliths send information to the lateral and inferior nuclei . Semicircular canals send information to the superior and medial nuclei.

236
Q

What general targets do the vestibular nuclei project to?

A
  • Spinal chord for maintenance of balance (neck and limb motor neurones)
  • Nuclei of the extraoccular muscles
  • Cerebellum
  • Cortex via the thalamus
  • Centres for cardiovascular and respiratory control
237
Q

Describe the central vestibular pathway for information from the otolith organs

A

Otolith organs –> lateral and inferior vestibular nuclei –> lateral vestibulospinal tract (which descends ipsilaterally in the VENTRAL FUNICULUS of the spinal chord –> axons terminate to influence motor neurones controlling muscles in the legs that help maintain posture.

238
Q

Describe the central vestibular pathway for information from the kinetic labyrinth (semicircular canals)

A

Semicircular canals –> medial and superior vestibular nuclei –> medial vestibulospinal tract descends down in the medial longitudinal fascilicus also connects to extraoccular motor neurones of CN III and VI to keep retinal image stationary.

239
Q

What are the vestibulo-collic and the vestibulo-spinal reflex?

A

The vestibulocollic pathway maintains the position of the head on the trunk. The vestibule-spinal reflex maintains the rest of the body in posture.

240
Q

How are the vestibular system and cerebellum connected?

A

Vestibular afferents from the vestibular ganglion and nuclei project to the cerebellar cortex - the flocculonodular lobe. Cerebellar efferents from the fastigal nucleus project to all vestibular nuclei.

241
Q

Via what thalamic nuclei do the vestibular nuclei project to the somatosensory cortex?

A

Ventral Posterior and Ventral Lateral nuclei

242
Q

Give an example of how the vestibular-occular reflex works (for when the head rotates anticlockwise.

A

This would require the eyes to move clockwise. Axons from the left horizontal canal innervates the left vestibular nucleus. This sends excitatory axons to the CONTRALATERAL abducens nucleus, which in turn excites the lateral rectus muscle of the right eye. Another excitatory projection from the abducens crosses the midline and ascends via the medial longitudinal fascilicus to excite the left oculomotor nucleus, which excites the left medial rectus muscle of the left eye.
To ensure speedy operation, the left oculomotor nucleus is also directly excited from the left vestibular nucleus. Speed is also maximised by inhibiting opposing movement.

243
Q

What results from malfunction of perception of movement in space?

A

Vertigo is the false perception that the world is spinning

244
Q

What results from malfunction of vestibulo-spinal reflexes?

A

Vestibular ataxia - instability of gait and posture

245
Q

What results from malfunction of vestibulo-occular reflexes?

A

Inability to stabilise eyes: vestibular nystagmus in unilateral lesions; oscillopsia during head movement in bilateral lesions

246
Q

What symptoms are associated with loss of vestibular function for gait?

A
  • If acute and uni-lateral, cases are associated with prominent vertigo, nausea and vomiting
  • If slow-onset and chronic bilateral, they may not have these characteristics, disequilibrium may be the side-resentation
247
Q

What is a result of a unilateral canal lesion?

A

The tonus of the intact canal gives a signal as if the head is rotating to the intact side - so patients experience symptoms of intense spinning.

248
Q

What are the common causes of vestibular vertigo?

A
  • Benign paroxysmal positional vertigo (BPPV) due to debris in canal causes intense vertigo and nausea for a few seconds. Most common.
  • Vestibular Neuritis caused by inflammation of ear. Lasts minutes to hours. Second most common cause. Continuous vertigo with obvious nystagmus.
  • Migrainous Vertigo
  • Meniere’s diseases can cause intense vertigo and nausea, hearing distrubance for hours. Rare.

Less common:

  • Infarction of labyrinth
  • Uncompressed vestibular lesion or stroke
  • Acoustic neuroma, tinnitus, hearing loss
249
Q

What is vestibular ataxia?

A
  • Bilateral vestibular disorder causes mild gait ataxia
  • Unilateral vestibular disorder causes the body to lean/ ‘fall’ on the lesioned side as the bonus of the intact one tells brain you’re falling on that side.
250
Q

What visual problems can arrise due to loss of vestibular function?

A
  • Vestibular nystagmus if unilateral: unopposed bonus of intact canal causes eyes to be driven to the lesioned side though VOR. Drifting movement detected by brainstem which resets eye positioning with fast saccades.
  • Oscillopsia (bilateral loss): impaired eye stabilisation so world is seen to bounce.
251
Q

What is the name of the eye socket?

A

The Orbit

252
Q

What is the diameter of the eyeball (globe)?

A

24mm

253
Q

What are the layers of tissue of the uvea?

A

Outer layer is the sclera, and forms the wall. Inside the sclera is the choroid, which is dark and has a red pigment. The inner layer is the retina, which has neurotissue.

254
Q

What defines the anterior and posterior segments of the eye ball?

A

Anterior segment can be described as the ocular structure anterior to the lens, with the posterior segment posterior to the lens.

255
Q

What are the who chambers of the eye?

A

The anterior chamber is between the cornea and the lens and is filled with Aqueous humour which supplies nutrients to surrounding cells.
The posterior chamber is filled with a jelly like substance called the vitreous humour which provides mechanical support.

256
Q

What are floaters?

A

The collagen and GAG chains of the vitreous humour can break down, presenting as floaters.

257
Q

What can cause a retinal tear?

A

An ageing vitreous humour.

258
Q

What is the ciliary body?

A

The ciliary body is a ring of tissue between the anterior and posterior segment of the eye, which bends the iris.

259
Q

What is the function of the ciliary body?

A

The ciliary body is the main engine for accommodation, and also secretes aqueous fluid.

260
Q

What is normal ocular pressure?

A

12-21 mmHg

261
Q

How does the ciliary body undergo accommodate the lens to increase its power?

A

The ciliary body supports the zonular fibres (suspensory ligaments) which attaches to the lens. On contraction, the ciliary body moves up and in and the zones are relaxed, allowing the lens to become more spherical –> increase in power.

262
Q

What is the purpose of the iris?

A

To regulate how much light enters into the eye. (Also gives eye ‘colour’)

263
Q

What terms describe pupil constriction and dilation?

A

Pupil contraction is Miosis; Pupil dilation is Mydriasis.

264
Q

What muscles achieve Miosis and Mydriasis?

A

Miosis is achieved by contraction of the sphincter papillae which are circular muscles in the eye.
Mydriasis is achieved by the contraction of dilator papillae which are radial muscles of the iris.

265
Q

What is glaucoma?

A

A group of diseases that presents with sustained intraocular pressure.

266
Q

What are the consequences of glaucoma?

A

Retinal ganglion cell death and can lead to optic disk cupping.

267
Q

What are the different types of glaucoma?

A
  • Primary open angle glaucoma (most common) is caused by a dysfunctional trabecular network (drainage system into the Canal of Schlemm). In this type there is normal-high IOP, but shows signs of glaucoma
  • Closed angle glaucoma is when increased pressure pushes iris/lens complex forwards, blocking the trabecular network leading to a cycle of increased pressure.
268
Q

What are the features of closed angle glaucoma?

A
  • Can be acute or chronic
  • Very rapid and painful + drop in vision + red eye
  • Risk factors include hypermetropia (small eye) and narrow angle at trabecular pressure
  • Can be treated with peripheral laser iridotomy to create drainage hole for iris.
269
Q

What are the components/anatomy of the lens?

A
  • Made of water (65%) and protein (35%)
  • Biconcave, elliptical and avascular
  • The outer acellular capsule envelopes the lens as a basement membrane.
  • The zones attach to the lens epithelium
  • The bulk of helens consists of regular inner elongated fibres, which only maintain transparency due to their regularity. With age, they lose their transparency, causing cataracts.
270
Q

What is the most common reversible cause of blindness?

A

Cataracts

271
Q

How much of the refractive power of the eye is the lens responsible for?

A

1/3

272
Q

What cranial nerve causes ciliary body contraction?

A

CN III

273
Q

What is the major refactoring surface of the eye?

A

The cornea (2/3 of refractory power)

274
Q

How does the lens change to accommodate for distant/near vision?

A

Distant - gets thinner

Near - gets fatter

275
Q

Describe the anatomy of the cornea

A
  • It is continuous with the sclera.
  • It has a convex structure.
  • It has 5 layers, absorbing UV
  • It has a tear film that supplies the cornea with oxygen.
276
Q

What are the layers of the tear film (covering the cornea)?

A

Has a superficial lipid layer to reduce evaporation. Below that is an aqueous layer, and below that a mucin layer.

277
Q

Why are tears produced?

A

Basal (keep the cornea with a supply of oxygen)
Reflex (in response to irritation)
Crying

278
Q

Where are tears produced, and where do they train to?

A

They are produced by the lacrimal gland. They drain through the superior and inferior canaliculi, gathering into the tear sacs before emptying into the tear duct.

279
Q

What structure of the eye prevents light from bouncing around?

A

The uvea (pigmented layer consisting of retina + chorioid + sclera)

280
Q

Describe the eyes of a person who does not need glasses

A

They have emmetropic eyes. Here parallel rays converge exactly on the retinal surface of the fovea, forming a clear image on the retina.

281
Q

What percentage of people are emmetropic?

A

80%

282
Q

Describe the eyes of those who need glasses

A
  • Hypermetropia (long sighted): Parallel rays focus behind the retinal surface, caused by a short globe or flat corneal surface
  • Myopia (short sighted): Distant objects focus in front of retinal surface. Glove too long, or high conner curvature.
283
Q

How can hypermetropia and myopia be corrected?

A
  • Hypermetropia with a convex lens

- Myopia with a concave lens

284
Q

What is the near response triad?

A
  • Sphincter pupillary contraction –> pupillary mitosis
  • Convergence of eyes by medi recti
  • Accommodation by circular ciliary muscle to increase refractive power. (Constriction to increase size of lens)
285
Q

What is presbyopia?

A

Naturally occurring loss of accommodation (less ability to see near objects).

286
Q

What is the physiological blind spot?

A

The optic disk, where the ganglion cells exit into the optic nerve.

287
Q

What is the area with the highest concentration of photoreceptors?

A

The macula

288
Q

What are the major blood vessels of the retina?

A
  • Superior-Temporal retinal artery (and vein)
  • Superior-Nasal retinal artery (and vein)
  • Inferio-temporal retinal artery (and vein)
289
Q

What is responsible for central vision?

A

The fovea

290
Q

What is the fovea?

A

A pit at the centre of the macula, which contains only cones (not ganglia as these are pushed aside).

291
Q

What are the uses for the two types of vision?

A

Central vision if used for reading, facts recognition etc.

Peripheral vision is used to recognise shapes and movement, as well as night vision.

292
Q

What tests assess central and peripheral vision?

A

Visual acuity assessment measures central vision

Visual field assessment measures peripheral vision

293
Q

Describe the macula

A

A pigmented region at the centre of the retina, about 6mm in diameter. It contains the fovea at the centre. The macula is also blood-vessel free as it absorbs blood from the choroid.

294
Q

How is blood supply to the retina split?

A
  • retinal blood vessels supply blood to the inner 2/3 of the retina.
  • the choroid supplies blood to the outer 1/3 of the retina (photoreceptors)
295
Q

Describe the layers of cells of the retina

A

Light ~~> Ganglion cells > Bipolar cells > Horizontal cells > Rods and Cones > Retinal epithelium > Choroid

296
Q

Describe the classes of photoreceptors in the retina

A
  • Rods: 100x more photosensitive; responsible for night vision; slow response to the light
  • Cones: less sensitive, but faster response; responsible for day light fine vision and colour vision.
297
Q

Describe the photoreceptor of the Rod cell

A

Rods contain the photo receptor rhodopsin. It is a transmembrane protein opsin with cofactor 11-cis-retinal. The cofactor reacts with a photon causing a conformational change –> action potential.
Reacts to blue-green light

298
Q

Describe the photoreceptor of the Cone cells

A

Cones contain 3 subtypes of photopsin that react to 3 light frequencies:
S-cone reacts to blue
M-cone detects green
L-cone detects red

299
Q

What is deutranomaly?

A

When two of the frequencies detected by rod cells combine. Most common form is M and L peak frequencies because they are already close to each other (leading to red-green confusion)

300
Q

What percentage of people have congenital colour deficiencies?

A

8% of males and 0.5% of females

301
Q

What test is used to assess colour blindness?

A

The ishihara test

302
Q

Describe the visual pathway

A

The ganglia of the outermost layer of the retina conduct action potentials to the brain via the Optic Nerve (CNIII). 53% of the nerve fibres cross at the optic chiasm.
Approximately 90% of the axons in the optic nerve go to the lateral geniculate nucleus in the thalamus via the retinogeniculostriate, where they synapse. Optic radiation cells transmit the impulses to the primary visual cortices.

303
Q

What are the different ordered neurones involved in the visual pathway?

A

1st order - rods and cones
2nd order - bipolar cells
3rd order - retinal ganglion cells
4th order - optic radiation cells

304
Q

How are the visual fields from both eyes made through the optic chiasma?

A

Only fibres from the nasal retina decussate, at the optic chiasma. This is responsible for the temporal visual field.
The uncrossed fibres originate from temporal retina and are responsible for the nasal field.
The criss-cross is due to the way light is reflected onto the retina.

305
Q

Where do the different visual fields project to the visual cortex?

A

The superior visual field projects to areas above the CALCARINE FISSURE, while the inferior visual fields below it. The right hemifield projects to the left primary visual cortex, and visa versa.

306
Q

Why does a stroke to the visual cortex usually present with contralateral homonymous hemianopia with macula sparing?

A

homonymous (same-side visual field) hemianopia (partial blind-ness) - so inability to see left or right visual field. Macula sparing as the area representing the macula in the cortex is disproportionally large, and has dual blood supply.

307
Q

What visual defect often accompanies pituitary tumours?

A

Bitemporal hemianopia as the tumour presses against the optic chiasm.

308
Q

What is the purpose for pupil constriction and dilation?

A

Constriction:

  • decrease glare and spherical aberrations
  • increases depth of field (near response triad)
  • reduces bleaching of photopigments

Dilation:

  • increases light sensitivity to the dark
  • aqueous humour drainage?
309
Q

What is the afferent pathway for the pupillary reflex?

A

Bipolar cells -> Pupil-specific ganglion cells exit at the posterior third of the optic tract before entering the lateral geniculate nuclei -> pretectal nucleus of the brainstem then the Eidinger-Westphal Nuclei on both sides

310
Q

What is the efferent pathway for the pupillary reflex?

A

Eidinger-Westphal nucleus –> Oculomotor nerve (CN III) –> Synapses at ciliary ganglion –> Short Posterior Ciliary Nerve –> Pupillary Sphincter

311
Q

What is the difference between direct light reflex and consensual light reflex?

A

The direct light reflex is the contraction of the pupil of the light-stimulated eye. The consensual light reflex is the contraction of the pupil of the other eye.

312
Q

How can a pupillary reflex afferent defect be detected?

A

Shining a light on the affected eye will not result in direct light reflex nor consensual light reflex but shining light on unaffected eye will result on both pupils constricting.

313
Q

How can a pupillary reflex efferent defect be detected?

A

The affected eye will not constrict whether any eye is stimulated. However, the normal eye will construct whether any eye is stimulated.

314
Q

What is a relative afferent pupillary defect, and how can you test for it?

A

This is when a partial pupillary response is still present when the damaged eye is stimulated.
Can be tested by winging the torch from eye to eye. You will be able to tell which eye elicits the weaker response as the pupils will paradoxically relatively dilate

315
Q

What nerves control the muscles controlling eye movement?

A

Occuolomotor Nerve: Superior, Inferior and Medial rectus + Inferior oblique muscle
Trochlear Nerve: Superior oblique
Abducens: Lateral rectus

316
Q

Define the following eye movement terms:

  • Convergence
  • Abduction
  • Adduction
A

Convergence is simultaneous adduction movement in both eyes when viewing a near object
Abduction is movement of the eye away from the midline
Adduction is movement of the eye towards the midline

317
Q

Define the following eye movement terms:

  • Supraduction

- Infraduction

A

Supraduction is elevation/movement upwards

Infraduction is depression/movement downwards

318
Q

Define the following eye movement terms:

  • Intorsion
  • Extorsion
  • Dextro and Levo
A

Intorsion is rotation towards the midline
Extortion is rotation away from the midline

Dextro (right) for Levo (left) can be used to describe the direction both eyes are looking at.

For example, dextroversion is looking right.

319
Q

Describe the features of third nerve palsy

A

The affected eye will look down and out
It will also have a droopy eye lid (as lid elevator is controlled by CN III)
This is because of unopposed superior oblique and lateral rectus muscles

320
Q

Describe the features of sixth nerve palsy

A

Affected eye unable to abduct and deviated inwards. Double vision worsens gazing to the side of the affected eye.

321
Q

Describe the features of internuclear ophthalmoplegia

A

This is due to damage to the medial longitudinal fascilicus. Right eye auction nor accompanied by left eye adduction. Also accompanied by nystagmus on right gaze.

322
Q

Define dizziness

A

The sensation of movement of self or environment. It is a non-specific term which can mean vertigo, light-headedness, weakness, unsteadiness etc.

323
Q

What is perceptuo-reflex uncoupling?

A

Plasticity to suppress dizziness by reducing the size of the vestibulocerebellum. This is why ballerinas don’t get dizzy.

324
Q

What should you check for in A&E when someone presents with vertigo?

A
  • Check postural blood pressure
  • Atrial saturation
  • ECG
    This is to make sure vertigo is not due to pulmonary embolism nor cardiac dysrhythmia.
325
Q

What are the core examinations for vertigo?

A
  • Eyes: cover, gaze testing, pursuit, saccades, VOR, fundoscopy
  • Ears: otoscope
  • Legs: gait
326
Q

What is the nystagmus type associated with vertigo?

A

Peripheral nystagmus, it may combine a rotational component with vertical and horizontal eye movements. NOT central nystagmus which is not due to a problem in the vestibular organ - it can result in up and down-beat nystagmus.

327
Q

What is it called when the VOR does not work?

A

Dolls Eyes

328
Q

What is oscillopsia?

A

A visual disturbance in which objects in the visual field appear to oscillate.

329
Q

What is the largest and most complex part of the cortex?1

A

The neocortex

330
Q

What are the different layers of the neocortex (and their general connections)?

A
  • Layer 1: molecular layer
  • Layer 2: external granular layer
  • Layer 3: external pyramidal layer
    Layers 1-3 mainly cortico-cortical connections. Layer 3 also connects to corpus callosum
  • Layer 4: internal granular layer
    Layer 4 receives input from the thalamus
  • Layer 5: internal pyramidal layer
  • Layer 6: multiform/fussiform layer
    Layers 5-6 have connections with subcortical, brain stem and spinal chord. Layer 6 also outputs to the thalamus.
331
Q

What has connections to all layers of the cerebral cortex?

A

The reticular activating system and the brainstem monoaminergic nuclei

332
Q

Describe the cortical processing of visual information

A

The primary cortical area receives the retinal input before information is passed on to the visual association area in the occipital lobe for higher level analysis. This analysis includes:

  • a ventral stream (what pathway) to the temporal lobe, which interprets form and colour
  • a dorsal stream (where pathway) to the parietal lobe which interprets spacial awareness.
333
Q

What is the inability to recognise familiar faces/learn new ones called?

A

Prosopagnosia

334
Q

What results from a lesion to the visual posterior association area?

A

Prosopagnosia

335
Q

What is the function of the frontal lobe?

A

The posterior part of the frontal lobe is involved in planning motor functions (premotor and primary motor cortex). The prefrontal association cortex is important in decision making, judgement, planning and foresight, basis for personality and appreciation of the self in relation to the world. Evidence also shows it is involved in restraining emotional functions.

336
Q

What is the function of the parietal lobe?

A

The anterior part of the parietal lobe is the primary somatosensory cortex. The posterior parietal association cortex is involved in creating a spacial map of the body in its surroundings.

337
Q

What can result from injury to the posterior parietal association cortex?

A

Disorientation, inability to understand spacial relationships, apraxia and hemispatial neglect (ignoring one side of the body/picture etc)

338
Q

What is the function of the temporal lobe?

A

Important in language (vernickle’s area), object recognition and more medially for the reconsolidating of memory and emotion (limbic system).

339
Q

What can result from injury of the temporal lobe?

A

Agnosia (disruption in object recognition), receptive aphasia (inability to understand language) and amnesia

340
Q

Describe usual hemispheric specialisation

A

The left hemisphere is more involved in writing, calculation etc. The right hemisphere is more involved in drawing, music etc

341
Q

What are the ways of studying cortical function?

A
  • study people with lesions
  • electron stimulation (lol)
  • measure brain activity with fMRI etc while being asked to perform a task
342
Q

What are the different white matter fibres in the brain?

A
  • Association fibres: Intracortical they connect cells in one area of the cortex within the same hemisphere. Long fibres include the superior longitudinal fasciculus and inferior longitudinal fascilicus.
  • Commissural fibres: Intracortical they connect corresponds cells in both hemispheres. Corpus callous interconnects frontal, parietal, occipital and some temporal, The rest of the temporal lobe is connected by the anterior commissure.
  • Internal capsule is extracortilal; passes through the base of the hemisphere connecting cerebral cortex with structures outside cerebral cortex.
343
Q

How many odours can the human olfactory system differentiate between?

A

2000-4000

344
Q

Where is our olfactory epithelium?

A

On the roof of the nasal cavity - the cribriform plate

345
Q

What cells make up the olfactory epithelium?

A
  • olfactory receptor neurones
  • substenacular/supporting cells (similar to glia and produce mucus
  • basal cells (the source of new neurones)
346
Q

How do olfactory receptor cells connect to the olfactory tract?

A

Axons from the olfactory receptor cells pass through perforations in the cribriform plate to enter the olfactory bulb. Here they synapse with mitral cells forming a glomerulus-like structure. The axons of the mitral cells form the olfactory tract.

347
Q

Describe the olfactory pathway in the brain

A

Olfactory tract divides into two olfactory striae:
- medial striae to the spatial nuclei
- lateral striae to the piriform cortex
The anterior commissure connects the two halves of the olfactory system instead of the corpus callosum.

348
Q

Where is olfactory information processed?

A

It is the piriform cortex and orbitofrontal cortex that processes olfactory information. They have connections to the brainstem and can promote autonomic responses

349
Q

Define anosmia

A

The clinical deficit in olfaction leading to the loss of sense of smell.

350
Q

What are the common causes of anosmia?

A

Trauma to the crirform plate. Neurodegenerative disorders like Alzheimer’s or Parkinson’s may show early pathology in the olfactory bulb.

351
Q

What is it called when an olfactory sensation preludes a seizure?

A

Prodromal aura

352
Q

What is the limbic system?

A

Structurally and functionally interrelated areas considered as a single functional cortex

353
Q

What is the function of the limbic system?

A
  • maintenance of the homeostatic response via activation of visceral effector mechanisms, modulation of pituitary hormone please and imitation of feeding and drinking
  • agonistic behaviour (defence and attacking)
  • sexual and reproductive behaviour
  • memory and learning
354
Q

What are the key structures of the limbic system?

A
  • Frontal lobe
  • Hippocampus (vital in memory)
  • Amygdala (responsible for fear and aggression)
  • Thalamus and various parts of the hypothalamus
  • Olfactory system feeds into the limbic system extensively
  • Septal nuclei
355
Q

Describe the Paper Circuit

A
  1. Hippocampus efferent is the fornix, which runs underneath the corpus callosum and comes down to terminate in the mamillary bodies at the base of the hypothalamus.
  2. From the mamillary bodies is the mamillothalamic tract which projects to the anterior nucleus of the thalamus. This causes emotional expression via the parasympathetic system (e.g sweating, changing pupil size)
  3. From the anterior nucleus of the thalamus there is a projection to the cortex lying immediately above the corpus callosum - the cingulate cortex (allows reactions to emotions to be coloured by previous experiences)
  4. From cingulate cortex there is a bundle of fibres that reinervates the hippocampus

The neocortex feeds into the cingulate cortex.

356
Q

What are the main afferent and efferent pathways of the hippocampus?

A

Main afferent is the perforant pathway to the enterorhinal cortex.
Main efferent is the fornix/fimbria

357
Q

Where does the hippocampus lie?

A

On the floor of the inferior horn of the lateral ventricle

358
Q

What is the function of the hippocampus?

A

Vital in laying down new memories and learning.

It is also responsible for the prodromal aura of epilepsy

359
Q

Where is the amygdala?

A

Next to the hypothalamus, buried in the white matter of the temporal lobe.

360
Q

What is the function of the amygdala?

A

Responsible for initiating fear and aggressive response, as well as flight and fight.

361
Q

What are the main afferent and efferent pathways of the amygdala?

A

Afferent: Olfactory cortex, septum, temporal neocortex, hippocampus and brainstem.
Main efferent: stria terminalis

362
Q

Describe the syndrome that arrises due to damage to both anterior temporal lobes

A

Kluver-Bucy Syndrome:

  • hyperorality
  • loss of fear
  • visual agnosia (inability to recognise objects)
  • hypersexuality
363
Q

Describe the progression of Alzheimer’s disease

A

Early:
- hippocampus and entorhinal cortex is where pathology starts –> short term memory loss

Mid:

  • Parietal love affected –> affects procedural memories
  • Dressing apraxia –> inability to get dressed

Late:

  • Frontal lobe affected
  • Loss of executive skills
364
Q

Describe the mesolimbic pathway

A

Dopaminergic pathway running from the substantia nigra to the basal ganglia.
Another small group of neurones in the tegmental area (midbrain) project to the cortex, nucleus accumbent and amygdala via the medial forebrain bundle. This pathway seems to be most important in drug dependence.

365
Q

Define consciousness

A

A cognitive process that enables us to experience the world around us.

366
Q

What system correlates with alertness of consciousness

A

The reticular activating system

367
Q

What is the reticular formation?

A

It is a polysynaptic network in the core of the midbrain, pons and upper medulla. It projects to the thalamus and cortex so it can control whether or not sensory signals reach cortical sites of conscious awareness like the frontoparietal cortex.

368
Q

What are the functions of the reticular formation?

A

It regulates many vital functions (such as cardiovascular, respiratory, bladder and motor patterns) and moderates the levels of consciousness.

369
Q

How does activity in the reticular activating system change with sleep?

A

There is always activity in the RAS. Specific sleep promoting pathways correlate with reduced reticular activating system (RAS) activity.

370
Q

Through what mechanisms does the reticular activating system use the thalamus?

A
  • Cholinergic neurones excite individual thalamic relay nuclei leading to activation of the cortex
  • Cholinergic projections to intralaminar nuclei, which in turn project to all areas of the cortex
  • Chlonergic projections to the reticular nucleus, which regulates flow of information through other thalamic nuclei to the cortex
371
Q

What nucleus in the hypothalamus is involved in maintaining a wake state?

A

Tuberomammillary nucleus (histaminergic) projects widely to cortex and is involved in maintaining wake state.

372
Q

How can different levels of arousal be detected?

A

Using an electroencephalogram (EEG)

373
Q

What are the five basic EEG rhythms?

A

1) Delta (0.5-4 Hz) present during sleep
2) Theta (4-8 Hz) associated with drowsiness
3) Alpha (8-13 Hz) subject relaxed with eyes closed
4) Beta (12-30 Hz) indicates mental activity
5) Gamma (~40Hz) associated with creation of conscious content in the minds eye.

374
Q

Define confusion

A

Confusion is a sustained disturbance of consciousness where mental processes are slow.

375
Q

What is the difference between stupor and a coma?

A

A state of stupor is a more profound state of confusion, which can only be roused by strong sensory stimuli.
A comma cannot be roused by even strong sensory stimuli. Different from sleep as metabolic activity in the brain is depressed and there is total amnesia for the period in coma.

376
Q

What is an international standard measure of levels of consciousness?

A

The Glasgow Coma Scale

377
Q

What can produce a coma?

A
  • metabolic alteration e.g hypoglycaemia, hypoxia, intoxication
  • lesions in cerebral hemispheres - only if massive and bilateral
  • lesions in thalamus or brainstem
378
Q

Describe the features of brain death

A
  • Irreversible coma due to brainstem death, but body can be kept alive artificially. Decision to cease treatment depends on demonstration of absence of brainstem reflexes and response to hypercapnia. Spinal reflexes and some postural movements may still be present.
379
Q

Describe the features of a persistent vegetative state

A

Irreversible coma due to disconnection of cortex from brainstem or widespread disease in cerebral hemisphere. Brainstem still functioning therefore reflexes, postural movements and sleep-wake cycle may still be present.

380
Q

What are the behavioural criteria of being asleep?

A
  • species specific posture
  • reduced responsiveness to external stimulation
  • minimal movement
  • reversible
381
Q

How can sleep be measured?

A

Using an electroencephalogram (EEG) electrooculogram (EOG) and an electromyogram (EMG)

382
Q

Describe the stages of sleep

A

Sleep stages 1-4 are non-REM sleep/slow wave sleep:

  • state changes gradually from drowsiness, through light sleep to deep sleep
  • the EEG shows gradual slowing from theta waves to delta
  • general muscle tone decreases gradually
  • relatively few eye movements

Sleep stage 5 is REM sleep:

  • EEG rhythm speeds up to Beta
  • General muscle tone becomes very low
  • Rapid eye movements occur
383
Q

When do dreams occur?

A

At any stage of sleep, but most prominent in REM sleep

384
Q

What systems are mainly active and less active during dreaming?

A

The limbic system is more active and the frontal cortex is less active.

385
Q

How long does a sleep cycle last for?

A

90 mins

386
Q

What nuclei are part of the reticular activating system?

A

The Raphe nuclei, nucleus coerules and cholinergic nuclei

387
Q

How does the hypothalamus control the activity in the RAS?

A

In a cyclical manner:
- Lateral hypothalamus promotes arousal
- Ventrolateral prophetic nucleus promotes sleep through inhibitory effects to RAS.
The two antagonistic nuclei alternate activity to regulate sleep-wake cycle as well as NREM/REM cycle.

388
Q

What structure in the pons is responsible for REM sleep?

A

The caudal pontine reticular formation is activated during REM sleep, to stress muscle tone and sensory input into the RAS, and activate eye movements (through superior colliculi) at the same time.

389
Q

Describe how our body has a circadian rhythm

A

Special retinal cells detect a decrease in light level and ACTIVATE the suprachiasmatic nucleus of the hypothalamus. This nucleus modules sleep-wake circuits, allowing you to get drowsy and sleepy. The SCN also has an endogenous biological clock and stimulates the pineal gland to secrete malting, which affects a range of physiological processes with day length.

390
Q

What evidence is there that supports the claim that sleep is necessary?

A
  • highly conserved through evolution
  • sleep deprivation is detrimental. performance decrements > concentration difficulty > energy management issues > hallucinations > death
  • sleep is regulated very accurately
391
Q

What are the function of sleep?

A
  • Restoration and recovery
  • Energy conservation
  • Predator avoidance
  • Memory consolidation
  • Other effects on brain function e.g dream are through to be important for dispersal of unwanted memories and a steam valve for antisocial emotions.
392
Q

Describe common sleep disorders

A

Insomnia (too little sleep) is highly prevalent:

  • in most cases causes transient effect on stress and emotional disturbance
  • some cases have physiological cause (sleep apnoea)
  • some causes due to psychological causes (depression)
  • treatment is to administer hypnotics - enhance GABAergic circuits

Narcolepsy (too much sleep) is when people enter REM sleep directly and repeatedly throughout the day. Often accompanied by cataplexy (sudden loss of muscle tone).

  • Genetic deficiency in orexin
  • Treatment is sleep management or stimulants