Neurology Flashcards

1
Q

What are the 2 principle pairs of arteries supplying the brain?

A

Internal carotid arteries and vertebral arteries.

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2
Q

Describe the circle of Willis.

A

An ‘orbital’ artery formed of many arteries. The 2 vertebral arteries converge to form the basilar artery, forming the posterior aspect of the circle. This bifurcates to from 2 posterior cerebral arteries. These give of posterior communicating arteries, which continue the circle of Willis. At the middle, the internal carotids join and give off a middle cerebral artery as a continuation. Anteriorly, the anterior cerebral arteries continue into the longitudinal fissure. The anterior communication artery links the 2 anterior cerebral arteries.

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3
Q

Describe the drainage of the cranium.

A

The cerebral veins drain into venous sinuses (made of folds of dura mater), which in turn drain into jugular veins.

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4
Q

Define stroke.

A

A cerebrovascular accident: a rapidly deteriorating focal disturbance of brain function of presumed vascular origin and of >24hours duration. Infarction 85% of cases, haemorrhage in 15% of cases.

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5
Q

Define transient ischaemic attack (TIA).

A

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

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6
Q

Describes the effects of an occlusion of an anterior cerebral artery.

A

Paralysis of contralateral leg (leg>arm). Disturbance of intellect, executive function and judgement. Loss of appropriate of appropriate social behaviour.

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7
Q

Describes the effects of an occlusion of a middle cerebral artery.

A

“Classic stroke” - contralateral hemiplegia (arm>leg), hemianopia.

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8
Q

Describes the effects of an occlusion of a posterior cerebral artery.

A

Visual defects (homonymous hemianopia), agnosia.

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9
Q

Describe the main causes of different types of haemorrhagic stroke.

A

Extradural (trauma, immediate effects)
Subdural (trauma, delayed effects)
Subarachnoid (ruptured aneurysms)
Intracerebral (spontaneous hypertensive).

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10
Q

Give common causes of syncope (fainting).

A

Manifestation of reduced blood flow to the brain: hypotension, postural changes, sudden pain, emotional shock.

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11
Q

Between which pressures is cerebral blood flow (CBF) autoregulated?

A

60-160mmHg

Autoregulation: intrinsic ability of the brain to maintain a constant blood flow despite changes in perfusion pressure.

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12
Q

How does CO2 cause vasodilation (and therefore increase blood flow) as part of local autoregulation (more CO2 is a result of more metabolic activity).

A

CO2 from the blood diffuses into the smooth muscle (H+ can’t cross the BBB). Here, it generates H+ using carbonic anhydrase. This increases the concentration of H+ (lowering pH) in the surrounding neural tissue and smooth muscle cells, which causes dilation.

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13
Q

What is the purpose of the BBB?

A

Protect the CNS from fluctuations in the composition of blood - as activity in neurones is highly sensitive to the composition of the local environment.

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14
Q

Which transporters are used to transport hydrophilic transporters across the BBB?

A

Water = AQ1, AQ4
Glucose = GLUT 1
Amino acids = 3 different transporters
Electrolytes = specific transporter systems.

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15
Q

What are the areas of the brain, usually near ventricles, which lack BBB collectively known as?

A
Circumventricular organs (CVOs). (They have fenestrated capillaries).
Usually involved in secreting into the circulation, or need to sample the plasma. 
The ventricular ependymal lining can be much tighter to limit exchange between them and the CSF.
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16
Q

Describe the differentiation of the neuroepithelium.

A

Neuroblasts: all neurones with cell bodies in the CNS.
Glioblasts: astrocytes; oligodendrocytes etc.
Ependymal cells: line ventricles and central canal.

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17
Q

What is the pial surface?

A

The boundary between grey matter and CSF.

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18
Q

Define brainstem.

A

The part of the CNS, exclusive of the cerebellum, which lies between the cerebrum and spinal cord.
Major divisions: medulla oblongata, pons, midbrain.
Sits in posterior cranial fossa.

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19
Q

How could you differentiate between different areas of the brain stem on imaging?

A

Midbrain: characteristic ‘mickey mouse’ shape, aqueduct, substantia nigra. Cerebral peduncle. Colliculi (posterior)
Pons: 4th ventricle and many transverse fibres. Middle cerebellar peduncle.
Medulla: 4th ventricle (diminished), pyramids, inferior olivary nucleus (wavy shaped). Inferior cerebellar peduncle.
Lower medulla: start of central canal, pyramidal decussation.

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20
Q

To which vertebral level does the dura mater extend?

A

S2

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21
Q

What is the epidural space?

A

A true space between the vertebral column and dura, filled with fat and venous plexus.

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22
Q

What is the additional, white filament present amongst cauda equina?

A

An extension of the pia mater tethering the spinal cord to the caudal end.

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23
Q

Where does discriminative touch, vibration and proprioception cross the midline?

A

Medulla.

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24
Q

Describe the location of the thalamus in relation to the ventricles.

A

Thalamus sits VENTRAL to the lateral ventricles, divided into two by the 3rd ventricle (N.B. ventral = inferior).

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25
Q

What is the only sensory system which doesn’t involve the thalamus?

A

Olfaction.

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26
Q

What do the intralaminar nuclei of the thalamus do?

A

Project to various medial temporal lobe structures (e.g. amygdala, hippocampus, basal ganglia). Mostly glutamatergic neurones.

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27
Q

What is the reticular nucleus?

A

The thalamic nucleus which forms the outer covering of the thalamus. The majority of its neurones are GABAergic. It doesn’t connect with distal regions but rather other thalamic nuclei. It received input and therefor acts to modulate thalamic activity.

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28
Q

What is the reticular formation?

A

A set of interconnected pathways in the brainstem which send ascending projections to forebrain nuclei (ascending reticular activation system (ARAS)). Involved in consciousness and arousal. Degree of wakefulness depends on ARAS activity.

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29
Q

What are the main functions of the hypothalamus colloquially?

A
The 4Fs
Fighting
Fleeing
Feeding
Fucking
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30
Q

What is the suprachiasmatic nucleus?

A

A hypothalamic nucleus which has connections to the pineal gland. It thus controls the secretion of melatonin and is involved in the circadian rhythm (sleep-wake cycles).

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31
Q

What is the paraventricular nucleus?

A

A nucleus of the hypothalamus which sends parvocellular and magnocellular neurones to the neurohypophysis.

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32
Q

Relate the 5 main cortices to their respective thalamic nuclei.

A

Motor cortices: ventral lateral and ventral anterior nuclei.
Somatosensory (body) cortex: ventral posterolateral
Somatosensory (head) cortex: ventral posteromedial
Visual: lateral geniculate
Auditory: medial geniculate

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33
Q

How would you distinguish between brainstem structures on imaging scans?

A

MIDBRAIN: has characteristic “mickey mouse” shape. Aqueduct present (only in midbrain), substantia nigra.

PONS: 4th ventricle, many transverse pontine fibres

UPPER MEDULLA: 4th ventricle (diminished), pyramids, inferior olivary nucleus (which has a wavy shape).

LOWER MEDULLA: starts of central canal, pyramidal decussation.

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34
Q

Describe the dorsal column-medial lemniscus pathway.

A

DCML is sensory, transmitting fine touch, vibration, 2-point discrimination and proprioception from the skin and joins to the primary somatosensory cortex in the parietal lobe. Axons from the lower body enter the dorsal column below T6 and travel in the gracile fasciculus (tract) to the gracile nucleus in the medulla. Axons from upper body enter at or above T6 and travel in the cuneate fasciculus to the cuneate nucleus. The neurons cross over at the sensory decussation in the medulla to form the medial lemniscus, which transmits the neurons to the ventral posterolateral (VPL) nucleus in the thalamus. The thalamus sends third order neurons to the primary somatosensory cortex (somatotopic representation).

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35
Q

Contrast thoracic and cervical spinal cord.

A

Cervical is larger and ovular, thoracic more circular.
Cervical has more white fibre tracts due to the converging of ascending and descending pathways.
Thoracic has intermediolateral cell column (preganglionic sympathetic neurons).
Below T6: no cuneate fasciculus.

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36
Q

What is a sensory receptor?

A

A transducer which converts energy from the environment into neuronal action potentials.

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37
Q

Which sensory receptors have free nerve endings and which have enclosed nerve endings?

A

Free nerve endings: thermoreceptors and nociceptors.

Enclosed nerve endings: mechanoreceptors.

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38
Q

Give 4 types of mechanoreceptors.

A

Meissner’s corpuscle: fine discriminative touch, low frequency vibration.
Merkel cells: light touch and superficial pressure.
Pacinian corpuscle: detects deep pressure and high frequency vibration.
Ruffini endings: continuous pressure or touch and stretch.

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39
Q

Define threshold.

A

The point of intensity at which the person can just detect the presence of a stimulus 50% of the time.

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40
Q

How does an increased stimulus strength / duration lead to greater intensity response?

A

More neurotransmitter is released.

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41
Q

What are tonic receptors?

A

Sensory receptors which do not adapt or adapt very slowly. They detect continuous stimulus strength, and continue to transmit impulses to the brain as long as the stimulus is present, keeping the brain constantly informed.
E.g. Merkel cells, which slowly adapt to allow superficial pressure and fine touch to be perceived.

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42
Q

What are phasic receptors?

A

Receptors which adapt quickly. They detect a change in stimulus strength, transmitting an impulse at the start and end of a stimulus (when a change is taking place).
E.g. the Pacinian corpuscle, where sudden pressure excites the receptor and it transmits a signal again once the pressure is released.

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43
Q

What is a receptive field?

A

A region of the skin which causes activation of a single sensory neuron when activated. Small receptive fields allow for the detection of fine detail over a small area (e.g. the fingers have densely packed mechanoreceptors with small receptive fields).

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44
Q

What are the two types of dorsal horn neurons?

A

Those with axons which project to the brain (projection neurons) and those with axons that remain in the spinal cord (interneurons).

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45
Q

Via what process is it possible to distinguish between 2 stimulus locations when receptive fields overlap?

A

Lateral inhibition, mediated by inhibitory interneurons within the dorsal horn of the spinal cord.

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46
Q

Describe the consequences of an anterior spinal cord lesion.

A

Blocked anterior spinal artery causes ischaemic damage to the anterior part of the spinal cord. Spinothalamic tract damage causes pain and temperature sensation loss below the level of the lesion.
Light touch, vibration and 2-point discrimination are retained due to intact dorsal columns.

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47
Q

Describe the first order neurons of the dorsal column-medial lemniscus pathway.

A

Sensory (AB) neurons in the dorsal root ganglia, which send afferent fibres trough the gracile and cuneate tracts to the gracile and cuneate nuclei in the medulla where they terminate and contact second order neurones.

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48
Q

Describe the second and third order neurons of the dorsal column-medial lemniscus pathway.

A

Second order neurons send fibres from the gracile and cuneate nuclei of the medulla to the ventral posterior lateral (VPL) nucleus of the thalamus.
Third order neurons are in the ventral nuclear group of the thalamus and send fibres to the primary somatosensory cortex of the parietal lobe.

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49
Q

What is the medial lemniscus?

A

The tract formed in the medulla by sensory decussation, which transmits the axons to the VPL nucleus of the thalamus.

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50
Q

Which first order neurons terminate in the cuneate nucleus and which terminate in the gracile nucleus of the medulla?

A

Axons from the lower body enter the dorsal column below T6 and travel in the gracile fasciculus (gracile tract) to the gracile nucleus.
Axons from the upper body enter at or above T6 and travel up the posterior column more laterally in the cuneate fasciculus (cuneate tract) to the cuneate nucleus.

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51
Q

Describe the spinothalamic / anterolateral pathway.

A

The tract via which pain and temperature sensation is transmitted.

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52
Q

Describe the first and second order neurons of the spinothalamic pathway.

A

First order neurons terminate in the dorsal horn of the spinal cord.
Second order neurons decussate immediately in the spinal cord and from the spinothalamic tract. These neurons terminate in the ventral posterior lateral (VPL) nucleus of the thalamus.

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53
Q

What are the different types of pain transmitted by A delta and C fibres?

A

A delta fibres mediate sharp, intense pain.
Type 1: noxious mechanical.
Type 2: noxious heat.

C fibres mediate dull, aching pain. Noxious thermal, mechanical and chemical stimuli.

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54
Q

Which tracts carry the “sensory” and “emotional” components of pain?

A

Sensory component = lateral spinothalamic tract.

Emotional component = spinoreticular tract.

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55
Q

Give an example of an ascending control pathway in nociception.

A

Gate-control theory.
Inhibition of primary afferent inputs before they are transmitted to the brain through ascending pathways, e.g. if you rub your elbow yourself.

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56
Q

What are the two types of chronic pain?

A

Nociceptive: noxious stimulation of a nociceptor (somatic or visceral).
Neuropathic: lesion or disease of the somatosensory system.

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57
Q

Mixed nociceptive and neuropathic chronic pain is commonest in which 2 conditions?

A

Lower back pain

Osteoarthritis.

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58
Q

Define allodynia and hyperalgesia.

A

Allodynia: pain due to a stimulus that doesn’t normally provoke pain.
Hyperalgesia: increased pain form a stimulus that normally provokes pain.

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59
Q

Define the term “motor unit”

A

A single motor neuron together with all the muscle fibres that it innervates. On average, each motor neurone supplies about 600 muscle fibres. Stimulation of one motor unit causes contraction of all the muscle fibres in that unit.

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60
Q

Which motor unit fatigues more quickly: a slow motor unit or a fatigue resistant fast motor unit?

A

A slow motor unit fatigues more slowly than the “fatigue resistance” fast motor unit.

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61
Q

Describe the slow motor unit.

A

Also called a ‘type 1’ motor unit. It has the smallest diameter cell body, smallest dendritic tree, thinnest axons and slowest conduction velocities of the 3 motor unit types. Most fatigue resistant and generates the lowest tension.

62
Q

Compare the two types of fast motor unit.

A

Fast, fatigue resistant (type 2A) has large diameter cell bodies, large dendritic trees, thicker axons and faster conduction velocity. Generates moderate tension.
Fast, fatiguable (type 2B) is the same, except not resistant to fatigue. Generates high tension.

63
Q

What are the types of motor units defined by?

A

The amount of tension generated, speed of contraction and fatigability of the motor unit.

64
Q

What is the size principle in recruitment?

A

Smaller units are recruited first (these are usually the slow twitch units). As more force is required, more units are recruited. This allows for fine control, under which low force levels are required. Derecruitment is the reverse order (smaller units last).

65
Q

What is rate coding in neuromuscular control?

A

Rate coding is where a motor unit can fire at a range of frequencies. Slow units fire at a lower frequency. As the firing rate increases, the force produced by the unit increases.

66
Q

What are neurotrophic factors?

A

A type of growth factor which prevents neuronal death and promotes growth of neurons after injury.

67
Q

Describe situations which facilitate the change of properties of fibre types.

A

Type IIA to type IIB motor unit most common following training.
Type I to II possible in cases of severe deconditioning or spinal cord injury.
Ageing associated with loss of type I and II with preferential loss of type II fibres.

68
Q

Describe the location and function of the primary motor cortex (M1).

A

Located in precentral gyrus of the frontal lobe, anterior to the central sulcus.
Functions include fine control and discrete, precise voluntary movement.

69
Q

What are the 2 descending motor pathways?

A

Lateral corticospinal pathway - which decussates in the medulla.
Anterior corticospinal pathway - which decussates in the spinal cord.
These travel in the lateral and anterior corticospinal tracts respectively.

70
Q

What is the premotor cortex?

A

A cortex found in the frontal lobe anterior to M1 (primary motor cortex) which is involved in the planning of movement. It regulates externally cued movement, such as seeing an apple and going to pick it up.

71
Q

What is the supplementary motor area?

A

Found anterior to the M1 in the frontal lobe, medially. Its function is planning complex movements; programming sequencing of movement. It regulates internally driven movement (speech).

72
Q

What are the negative and positive signs associated with an upper motor neuron lesion?

A

Negative sign = loss of function = paresis/paralysis.
Positive sign = increased abnormal motor function due to loss of inhibitory descending inputs: spasticity (increased muscle tone); hyper-reflexia, Babinski’s sign.

73
Q

Define apraxia

A

A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements. Lesion of inferior parietal lobe/ frontal lobe.

74
Q

Give signs associated with lower neuron lesion.

A

Weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculations (damaged motor units produce spontaneous action potentials), fibrillations (spontaneous contraction of individual muscle fibres).

75
Q

What is motor neuron disease?

A

A progressive neurodegenerative disorder of motor system. It is a spectrum of disorders.

76
Q

What are some of the components of the basal ganglia/

A

The caudate nucleus and lentiform nucleus (putamen + external globus pallidus) and nucleus accumbens, striatum.

77
Q

Define reflex.

A

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

78
Q

What are the main motor signs of Parkinson’s disease?

A

Bradykinesia, hypomimic face (expressionless, mask-like), akinesia, rigidity, tremor at rest (starting in one hand).

79
Q

What is the cause of Huntington’s disease?

A

A chromosome 4 autosomal dominant abnormality where there are excessive CAG repeats leading to the degeneration of GABAergic neurons in the striatum: caudate and then putamen.

80
Q

What are the signs of Huntington’s?

A

Choreic movements: rapid, jerky, involuntary movements of the body, hands and face first then the legs and rest of the body.

81
Q

What are the 3 divisions of the cerebellum and their functions?

A

Vestibulocerebellum: regulation of gait, posture and equilibrium. Co-ordination of head movements with eye movements.
Spinocerebellum: coordination of speech, adjustment of muscle tone, coordinates limbs.
Cerebrocerebellum: coordination of skilled movements, cognitive function, attention and processing of language.

82
Q

What are the criteria of an activity being classified as sleep?

A

Species-specific posture, minimal movement, reduced responsiveness to external stimuli and reversible with stimulation (unlike coma, death, anaesthesia).

83
Q

What structures in the brain are involved with sleep?

A

Reticular activating system (RAS) - controls consciousness.
Hypothalamic nuclei:
Lateral hypothalamus (LH) - promotes wakefulness (secretes orexin/ hypocretin).
Ventrolateral preoptic nucleus (anterior hypothalamus) - promotes sleep.
Suprachiasmatic nucleus - synchronises sleep with falling light levels - involved with melatonin.

84
Q

What changes to sleep do you get after sleep loss?

A

Reduced latency to sleep onset.
Increase of slow wave sleep (NREM).
Increase of REM sleep (after selective REM deprivation).

85
Q

Give some theories for the function of sleep and why they are unlikely to be correct.

A
Restoration and recovery - unlikely since active people don't sleep more. 
Energy conservation (10% drop in BMR) - unlikely since there is no benefit in terms of energy consumption over lying still.
Predator avoidance - unlikely since so complex.
Recent research suggests memory consolidation and other cognitive faculties.
86
Q

What may the functions of dreams be and when do we dream?

A

We dream in both REM and NREM sleep, just more frequently in REM sleep.
Contents of dreams are more emotional than ‘real-life’ - since brain activity in limbic system higher than in frontal lobe during dreams.
Functions - safety valve for antisocial emotions; disposal of unwanted memories; consolidation.

87
Q

Detail insomnia’s prevalence, causes and treatment.

A

High prevalence, most cases transient.
Causes of chronic cases can be physiological (sleep apnoea, chronic pain) or brain dysfunction (depression, fatal familial insomnia, night working).
Treatment - sleep hygiene, hypnotics (enhance GABAergic receptors), CBT.

88
Q

Give examples of good sleep hygiene.

A
Going to bed and waking up at fixed times.
Creating a relaxing bedtime routine. 
Only going to bed when you feel tired.
Avoiding caffeine/alcohol at night
Not napping.
No heavy meals.
No phones or screen before bedtime.
89
Q

What is hypersomnia.

A

Excessive daytime sleepiness.
Primary causes - narcolepsy, post-traumatic brain injury.
Secondary hypersomnia (poor sleep), due to obstructive sleep apnoea, nocturnal pain, neurodegenerative disease, medication, anxiety and environment.

90
Q

What is narcolepsy?

A

Falling asleep repeatedly in the day and disturbed sleep at night. A cause of primary hypersomnia.
Can be associated with cataplexy - sudden, loss of voluntary muscle tone, often triggered by strong emotion (e.g. laughing).
Dysfunction of control of REM sleep. Orexin/ hypocretin deficiency.

91
Q

Which two structures are involved with consciousness?

A
Reticular activating system - enables consciousness.
Reticular formation (RF) - regulates vital functions. Degree of activity is associated with alertness. RF projects to hypothalamus, thalamus and the cortex.
92
Q

What is a coma?

A

A state of unrousable unresponsiveness, lasting >6 hours. Can’t be awakened, fails to respond normally to painful stimuli, sound or light, no voluntary actions initiated, lacks normal sleep cycle.

93
Q

What is a vegetative state?

A

Wakefulness without awareness. Preserved capacity for spontaneous or stimulus-induced arousal, evidenced by sleep-wake cycles and a range of reflexive and spontaneous behaviours. Characterised by complete absence of behavioural evidence for self- or environmental-awareness.

94
Q

What is a minimally-conscious state?

A

A severely altered consciousness in which minimal but clearly discernible behavioural evidence of self or environmental awareness is demonstrated. Characterised by inconsistent, but reproducible, responses above the level of spontaneous or reflexive behaviour, which indicated some decree of interaction with their surroundings (e.g. track someone with their eyes).

95
Q

Give causes of coma.

A

Metabolic - drug overdose, hypoglycaemia, diabetes, hypercalcaemia.
Intracranial - head injury, meningitis, encephalitis, epilepsy, hypoxic brain injury.
Brain stem - infarct, tumour, abscess
Hemisphere lesion - cerebral infarct, haemorrhage, abscess or tumour.

96
Q

What 3 types of fibre can cerebral white matter be divided into?

A

Association fibres: connect fibres within the same hemisphere
Commissural fibres: connect left and right hemisphere
Projection fibres: connect cortex with lower brain structures (e.g. thalamus, brainstem and spinal cord).

97
Q

Describe the neocortex.

A

6 layer structure of grey matter.
Layers I-III mainly cortico-cortical connections. Layer I acellular.
Layer IV - input from thalamus
Layers V and VI, connections with brainstem and spinal cord.
Arranged in layers (laminar structure) and columns.
Neurons with similar properties are connected in same column.

98
Q

Give the main differences between primary and association cortices.

A

Primary cortices have predictable have predictable functions, are organised topographically and have left-right symmetry.
Association cortices have less predictable function, aren’t organised topographically and left-right symmetry is weak or absent.

99
Q

What symptoms are associated with frontal cortex lesions?

A

Lack of planning, behaviour becomes disorganised, attention span and concentration diminish, self-control hugely impaired.

100
Q

What symptoms are associated with parietal cortex lesions?

A

Posterior parietal association cortex creates a spatial map of the body in surroundings. Injury may cause disorientation, inability to read maps or understand spatial relationships, apraxia.

101
Q

What symptoms are associated with temporal cortex lesions?

A

Agnosia, receptive aphasia. (Temporal cortex lesions involved with language, object recognition, memory, emotion).

102
Q

What does diffusion tensor imaging (tractography) - a modality of MRI look at?

A

Shows integrity of pathways.

103
Q

What do MEG, EEG and fMRI scans looks at?

A

MEG and EEG measure magnetic and electric fields respectively.
fMRI looks at blood flow in brain as a marker of activity.

104
Q

What is the difference between transcranial magnetic stimulation and transcranial direct current stimulation?

A

Transcranial magnetic stimulation: the magnetic field induces an electric current in the cortex, causing neurons to fire. This can be used to test whether a specific brain area is responsible for a function.

Transcranial direct current stimulation changes the local excitability of neurons, increasing or decreasing firing rate (doesn’t directly stimulate neurons).

105
Q

What are the 1st, 2nd and 3rd order neurons in the visual system?

A

1st order: rod and cone retinal photoreceptors.
2nd order: retinal bipolar cells
3rd order: retinal ganglion cells –> optic nerve –> partial (53%) decussation at optic chiasm.

106
Q

What is the receptive field of a neuron?

A

Region of skin which causes activation of a single sensory nerve when stimulated.
In the eyes, it is the retinal space within which incoming light can alter the firing pattern of a neuron.

107
Q

What is the relationship between convergence and receptive fields? (in the eyes)

A

Low convergence: small receptor field: fine visual acuity: low light sensitivity.
Cone system convergence < rod system convergence
Central retina convergence < peripheral retina convergence.

108
Q

What is an off-centre ganglion?

A

Inhibited by light at centre of receptive field, stimulated by light at edge (opposite of on-centre ganglion).
Important for contrast sensitivity and enhanced edge detection.

109
Q

Which fibres at the optic chiasm are responsible for which visual field and how does the position of a lesion affect its effect on vision?

A

Crossed fibres - originating from nasal retina - are responsible for temporal visual field.
Uncrossed fibres - originating from temporal retina - responsible for nasal visual field.
Lesion at optic chiasm = bitemporal hemianopia. Usually an enlarged pituitary gland.
Lesion posterior to optic chiasm = homonymous hemianopia in both eyes on same side (e.g. right-sided lesion causes left-sided homonymous hemianopia in both eyes). Usually a stoke or cerebrovascular accident.
Lesion anterior to optic chiasm = affects visual field in one eye only.

110
Q

How does macula-sparing homonymous hemianopia arise?

A

Since the area in the primary visual cortex being disproportionately large and receiving a dual blood supply from posterior cerebral arteries from both sides. (Damage to primary cortex usually stroke).

111
Q

What is the extrastriate cortex?

A

Area surrounding visual cortex in occipital lobe. Converts basic visual info into orientation and position.
Dorsal pathway = motion detection, visually guided action (“where?”)
Ventral pathway = object representation, facial recognition (“what?”)

112
Q

What do the dorsal and ventral visual pathways convey?

A

Dorsal pathway = motion detection, visually-guided action.

Ventral pathway = object representation, face recognition.

113
Q

Describe the pupillary reflex.

A

Pupil constriction mediated by parasympathetic nerve (CN III). Dilation = sympathetic nerve.
CNII - optic nerve - optic chiasm - optic tract - lateral geniculate nucleus (thalamus) –> optic radiation –> primary visual cortex.
In reflex, efferent pathway from each eye synapses on Edinger-Westphal Nucleus in midbrain.
Edinger-Westphal Nucleus –> oculomotor nerve efferents to both eyes, hence both eyes constrict when you shine light in one eye.
Direct (ipsilateral) light reflex = constriction of pupil of light-stimulated eye.
Consensual light reflex = constriction of pupil of fellow eye.

114
Q

What is the limbic system and its functions?

A

A rim, or limbus, of cortex adjacent to corpus callosum & diencephalon.
Structurally and functionally interrelated areas considered a single functional cortex.
Responsible for processes aimed at survival of the individual: maintenance of homeostasis, memory, agonistic behaviour, sex and reproduction.

115
Q

What is the Papez Circuit?

A

A neural circuit for the control of emotional expression. Links the hypothalamus and limbic system.
Hippocampus feeds into the circuit with emotional colouring (previous experience) relaying info to the mamillary bodies of the hypothalamus via the fornix. Hypothalamus provides emotional experience (new experience), feeds into anterior nucleus of thalamus, which conveys to cingulate cortex providing emotional expression (response).

116
Q

Briefly give the anatomical progression of Alzheimer’s disease.

A

Early. Hippocampus and entorhinal cortex, short-term memory problems.
Moderate. Parietal lobe; dressing apraxia.
Late. Frontal lobe, loss of executive skills.

117
Q

What is the amygdala?

A

A grey-matter nucleus in white-matter temporal lobe, just anterior to hippocampus.
Functions are fear and anxiety and fight or flight.
Kluver-Bucy syndrome leads to loss of fear, hypersexuality and agnosia. Also hyperorality (putting things in the mouth).

118
Q

Briefly give the simplistic mechanism of drug dependence.

A

Opioids, nicotine, amphetamines, ethanol and cocaine all increase dopamine release in nucleus accumbens.
Stimulate midbrain neurons, promote DA release or DA reuptake inhibition
Addiction.

119
Q

What is the role of the ossicles?

A

They transmit the vibration of the tympanic membrane onto the oval window of the cochlea. They match the impedance (reluctance of a system receiving energy from a source) and reduce the loss in energy as the vibration goes from air to cochlea.
The frequency at which impedance is minimal is the resonant frequency.
The position of the malleus and incus can be adjusted by the tensor tympanic muscle & stapedius muscle to control tension of the tympanic membrane.

120
Q

What is conductive hearing loss?

A

Where the ear is not capable of transmitting the vibration of sound waves onto the cochlea.
In children, fluid accumulation in the inner ear (otitis media) is a common cause.
A perforated tympanic membrane is a form of conductive hearing loss.
Barotrauma is a temporary cause.
An abnormal growth of bone (e.g. otosclerosis) can obstruct the ear canal.

121
Q

How does the basilar membrane (lining the cochlea) break down complex sounds?

A

It is an elastic structure that vibrates at different positions along its length in response to different frequencies.
Narrow, tough at base, broad and floppy at apex.
Distributes the energy of each component frequency along its length to build a tonotopic map.
The motion of the basilar membrane deflects the hair bundles of hair cells.

122
Q

Describe the active process of audition.

A

Stereocilia (microvilli-like projections on hair cells) are connected by filamentous linkages called top links. They work as small springs stretched by the sliding of the stereocilia.
Response currents result from the opening of ion channels activated by stretching of top links.
The opening of mechanically-activated ion channels in response to an external stimulus relaxes the top link, and in turn, the whole hair bundle. A healthy hair bundle actively complies with the direction of the stimulus.

123
Q

Compare and contrast inner and outer hair cells.

A

Inner hairs cells (1 row) roughly 3500 per human cochlea.
Outer hair cells (3 rows) roughly 11,000 per human cochlea.
95% of afferent projections project form IHCs. IHCs provide sensory transduction.
Most of the efferent projections connect to OHCs.
OHCs cell bodies shorten and elongate when their internal voltage is changed (electromotility).
Electromotility due to the reorientation of the protein PRESTIN.

124
Q

How is the tonotopic map continued beyond the basilar membrane?

A

Hair cells form synapses with sensory neurones in the cochlear ganglion. Each ganglion responds best to stimulations at a particular frequency.
Arrives at ventral cochlear nucleus. Low frequencies ventrally. High frequencies dorsally.

125
Q

What is sensorineural hearing loss?

A

When the problem is rooted in sensory apparatus of the inner ear or the vestibulocochlear nerve.
Presbycusis (age related hearing loss)
Caused by loud noises (military, industry, clubs, loud headphones)
Genetic mutations (e.g. hereditary disorders affecting the organ of Corti).
Meniere’s disease
Toxicity (E.g. aminoglycoside antibiotics)
Hearing loss primarily due to loss of hair cells (which don’t regenerate in mammals).
Also, acoustic neuroma, demyelination in MS.

126
Q

How do cochlear implants work?

A

An elongated coil is interested into the cochlea with pairs of electrodes corresponding to signal frequencies.
Sends the signal to the auditory nerve via antennas.
Bypasses the dead hair cells and simulates the nerve fibres directly.
Early models had 4 channels. 20 channels needed to understand speech well. No active process.

127
Q

Which structures locate sounds in the vertical and horizontal planes?

A

Dorsal cochlear nucleus locates sounds in the vertical plane using info from the ventral cochlear nucleus.

Superior olivary complex (SOC) locates sounds in horizontal plane by comparing the bilateral activity of the cochlear nuclei.
Medial superior olive computes the interaural time difference. A map of interaural delay can be formed due to delay lines.
Lateral superior olive detects difference in intensity between 2 ears.
Neurons are excitatory (ipsilateral) and inhibitory (contralateral) in SOC.

128
Q

What is the role of the inferior colliculus?

A

All ascending auditory pathways converge here.

Inferior colliculus carries info about sound localisation: precedence effect - filtering out unnecessary sounds.

129
Q

What happens at the superior colliculus?

A

Auditory and visual maps merge. The auditory map is essential for reflexes for orienting the head and eyes to acoustic stimuli.

130
Q

What is the role of the primary auditory complex (A1)?

A

Gaze control in response to complex tasks.

131
Q

What are the inputs and outputs of the vestibular system?

A

Inputs: visual, rotation and gravity (ear),
Outputs: ocular reflex, postural control, nausea.

132
Q

Describe the vestibular system in the ear.

A

Located in the labyrinth (inner ear) in the temporal bone.
Saccule and utricle (connected together) and semi-circular canals (connects to utricle).
Each semi-circular canal has an ampulla.
Posterior, lateral and anterior semi-circular canals (all 45 degrees apart).

133
Q

What is the role of the saccule and utricle (otolith organs)?
NB the otolith organs are known as the static labyrinth.

A

Saccule detects vertical movement.
Utricle detects horizontal movement.
The saccule and utricle have maculae (saccule’s macule is vertical in orientation and measures vertical acceleration). Hair cells located at maculae.
A gelatinous matrix moves the hairs as liquids are not dense enough. Otoliths (carbonate crystals) also present.
The striola is the central region of the macula. The hair bundles are in opposite orientations either side of the striola.

134
Q

What is the kinetic labyrinth?

A

Semi-circular canals. In semi-circular canals, hair cells are only located in ampulla. Also has gelatinous matrix (capula).
The other parts of the semi-circular canals contain endolymph, which moves in the opposite direction to the direction of head movement.
The SCCs work in pairs.

135
Q

What are the vestibulocochlear pathways?

A

Primary afferents end in vestibular nuclei and in cerebellum.
Vestibulocochlear pathways –> movement coordination, posture regulation.
Functions: to detect and inform about head movements.
Keep images fixed on the retina during head movements. Postural control.

136
Q

What is meant by the term resting discharge?

A

Hair cells in the vestibular system are always discharging. Depolarisation increases frequency of discharge. At constant velocity = resting discharge.

137
Q

Which pairs of SCCs work together?

A

Both horizontal (lateral).
Left anterior - right posterior (LARP)
Right anterior - left posterior (RALP)
One inhibited, one excited.

138
Q

Why don’t otolith organs work in pairs?

A

They have inbuilt redundancy. The hair bundles are in opposite orientation either side of the striola.

139
Q

What is the vestibuloocular reflex?

A

Quickest reflex in body (5-7msec).
Keeps images fixed.
Eye movement in opposite direction to head movement.
Connection between vestibular nuclei and oculomotor nuclei.
Contralateral abducens nucleus (to abduct opposite eye)
Then contralateral oculomotor nucleus (to adduct other eye)

140
Q

What’s the difference between a peripheral and central vestibular disorder?

A

Peripheral vestibular disorder involves labyrinth and VIII nerve.
Central vestibular disorders involve CNS (brainstem/ cerebellum).

141
Q

How do you test a lesion anterior of the optic chiasm affecting afferent conduction?

A

Right afferent defect e.g. damage to optic nerve.
No pupil constriction in either eye when right eye is stimulated by light. Both eyes constrict when left eye is stimulated by light.
Unilateral afferent defect = different response depending on which eye is stimulated.

142
Q

How do you test a lesion anterior of the optic chiasm affecting efferent conduction?

A

Right efferent defect e.g. damage to oculomotor.
No right pupil constriction whether right or left eye stimulated with light.
Left eye pupil constriction whether left or right eye stimulated.
Unilateral efferent defect = same unequal response between left and right irrespective of which eye is stimulated.

143
Q

What is the swinging torch test?

A

Tests relative afferent pupillary defect.
Partial pupillary response still present when the damaged eye is stimulated.
Swinging torch test = alternating stimulation of right and left eye with light.
Both pupils constrict when light swings to left undamaged eye, Both paradoxically dilate when light swings to right damaged eye.

144
Q

What is meant by duction?

A

Eye movement in one eye

145
Q

What is meant by version and vergence?

A

Version: Simultaneous movement of both eyes in same direction.
Vergence: Simultaneous movement of both eyes in opposite directions.

146
Q

Define convergence.

A

The simultaneous adduction in both eyes when viewing a near object.

147
Q

What is saccade?

A

Rapid movement of the eye between fixation points. Short-fast bursts of up to 900/s.
Reflexive saccade to external stimuli.
Scanning saccade.

148
Q

What do the superior and inferior branches of the oculomotor nerve supply?

A
Superior = superior rectus + LPS.
Inferior = inferior and medial recti, inferior oblique and pupil constriction.
149
Q

How do you test extraocular muscles?

A
Abduction = lateral rectus
Adduction = medial rectus
Elevated and abducted = superior rectus.
Depressed and abducted = inferior rectus
Elevated and adducted = inferior oblique
Depressed and adducted = superior oblique
150
Q

Give signs of third nerve palsy.

A
Affected eye depressed and abducted (down and out).
Droopy eyelid (ptosis).
151
Q

Give signs of sixth nerve palsy.

A

Affected eye unable to adduct and deviates inwards.

Double vision worsens on gazing to the side of the affected eye.

152
Q

Describe special adaptations of the BBB.

A

The capillaries have extensive tight junctions at the endothelial cell-cell contacts, have dense pericyte coverage (as opposed to the sparse coverage of peripheral capillaries) and are covered with “end feet” from astrocytes.