B06W11 Flashcards Preview

Block 6: Neuro > B06W11 > Flashcards

Flashcards in B06W11 Deck (401):
1

What is the difference between endolymph and perilymph?

Perilymph like extracellular fluid and endolymph like intracellular fluid > allows for conduction of actin potential through movement of ions

2

Each inner hair cell of the ear has terminals for how many afferent fibres?

20

3

What mechanical stimulus leads to depolarisation of the ear inner hair cells?

Distortion of the stereocilia

4

Which structure of the ear generates the active mechanical amplification of basilar membrane vibration?

Outer hair cells

5

What are the 4 components of clinical assessment of hearing?

1. History 2. Clinical testing 3. Tuning forks 4. Audiometry

6

List 3 associated symptoms of hearing loss that may be elicited in a history

Tinnitus, hyperacusis and vertigo

7

Inner hair cells are ____ nerve fibres

Afferent

8

What is the role of inner hair cells in the ear?

Transmission of information to auditory nerve

9

What do outer hair cells in the ear do?

Generate the active mechanical amplification of basilar membrane vibration, leading to large amplitude and sharply tuned mechnical travelling wave

10

Outer hair cells produce what types of otoacousticemissions?

Spontaneous and evoked

11

Problems with hearing fall into which 2 major groups? Give an example of each.

1. Mechanical delivery (conductive) as in otitis media with effusion 2. Neurological (sensorineural) as in noise induced hearing loss

12

In a Weber's tuning fork test, sound will deviate towards the affected ear in ____ hearing loss, but away from the affeted ear in ______ loss

Conductive; sensorineural

13

The inner ear labyrinth consists of which 3 parts?

Urticle, saccule and 3 semicircular canals

14

List the 3 planes of movement in the inner ear labyrinth

Yaw, pitch and roll

15

Describe how the ear perceives acceleration in a clockwise direction

Clockwise acceleration > inertia causes endolymph to lag behind > cupula gets deflected toward the right > perceived clockwise movement

16

Describe how the ear perceives deceleration

Canal stops moving but endolymph momentum keeps it moving clockwise > cupula becomes deflected

17

In which 2 situations does the ear not perceive any angular movement?

Constant angular motion and at rest, because in these situation there is no relative motion between the canals and the endolyph, so the cupula is not deflected and there is no perception of movement

18

Decscribe Ewalds 3 laws

1. Stimulation of a semicircular canal causes a movement of the eyes in the plane of the stimulated canal 2. In the horizontal canal, ampullopetal endolymph flow causes greater response than ampullofugal flow 3. In vertical canals, ampullofugal endolyph flow causes greater response than ampullopetal flow

19

Each utriculopetal stimulus in one ear canal is matched by an equal but opposite ______ displacemnt in the functionally paired canal

Utriculofugal

20

What is nystagmus?

Combination of alterating slow phase and fast saccadic eye movements in opposite directions

21

For clinical purposes, the direction of nystagmus is defined by which phase?

Fast

22

List the 5 important tests of vertigo

1. Rhombergs 2. Unterbergers (contentious value) 3. Head thrust (vestibulo-occular test) 4. Hallpikes 5. Caloric responses

23

What systems are tested using Rhomberg's test?

Vestibular, proprioception and cerebellum

24

When conducting Rhomberg's test, a patient will tend to fall to the side of _____ labyrinth

Weak

25

Which test is used for unilateral vestibular hypofunction?

Head thrust test

26

What is the specific test for benign paroxysmal positional vertigo?

Hallpikes test

27

Which 4 skills and 4 lobes are tested in a neuro exam of higher cognitive function?

Orientation, language, attention and memory. Frontal, parietal, temporal and occipital lobes.

28

Which 4 nerves are tested in the exam of the UPPER cranial nerves?

II, III, IV, VI

29

What does CNI do?

Sense of smell

30

How is CNI tested in an exam?

Ask patient about their sense of smell or ask patient to smell a strong scent one nostril at a time (only seeing if patient can detect the smell, not if they can identify it)

31

What are the functions of CNII?

Vision

32

Which tests are used to test CNII?

Visual acuity, visual fields, ophthalmoscopy and pupil reactivity

33

What are the sympathetic functions of CNII?

Pupillary dilation, lid elevation, facial sweating

34

What sort of visual field defect would be produced by a lesion of the right optic nerve?

Total visual loss in the right eye, but normal vision in the left

35

What sort of visual field defect would be produced by a lesion of the right-most side of the optic chiasm?

Loss of central vision in the right eye and loss of the upper outer quadrant of the left eye

36

What sort of visual field defect would be produced by a lesion of the central optic chiasm?

Loss of lateral field in the right eye and lateral field of the left eye

37

What sort of visual field defect would be produced by a lesion of the right optic tract? (i.e., behind the optic chiasm on the right)

Loss of nasal half of field in right eye and loss of temporal half of field in left eye

38

What sort of visual field defect would be produced by a lesion spanning the entire right optic radiators (in the primary visual cortex)?

Loss of nasal half of field in right eye and loss of temporal half of field in left eye

39

List a test of colour vision

Ishiara plates

40

Why is documentation of visual fields different from any other documentation of eye function?

These are drown as if patient were looking into the page (i.e., right eye on right side)

41

A deep space-occupying lesion in the orbit can cause what sign?

Proptosis

42

How are eyelids examined in a cranial nerve examination?

Ask patient to look up, straight ahead and down.

43

ist at least 3 conditions in which an abnormality of eyelids may be seen

1. Occulomotor nerve palsy 2. Horner's syndrome 3. Senile dehlescence 4. Myasthenia gravis

44

List the 3 planes of movement of the eyeball

1. Horizontal 2. Vertical 3. Tortionally

45

From the adducted position, what are the actions of the inferior oblique and superior oblique?

Inferior oblique elevates the eye, superior oblique depresses the eye

46

What is the difference between elevation and depression of the eyeball when in the abducted vs adducted position?

Abducted position = superior rectus elevates and inferior rectus depresses; Adducted position = inferior oblique elevates and superior oblique depresses the eye

47

What 4 features are observed when examining the pupils in a cranial nerve exam?

1. Direct 2. Consensual 3. RAPD 4. Convergence

48

What sort of defect can be elicited by using the 'swinging torch test' in a cranial nerve exam?

Realtive afferent puillary defect

49

Which branch of CNV is the motor branch?

Mandibular

50

Which tests are used to test CNV?

Facial sensation, corneal reflex, jaw movements and jaw jerk

51

What is the function of CNV?

Sensory to face and ear, and muscles of mastication

52

Why is vibration sense useless in testing CNV sensation to the face?

Because the skull will transfer the vibration to both sides

53

Which muscles open the jaw and move it from side to side and protrude?

Pterygoids

54

Why is a patient asked to look up and away from cotton wool in the corneal test (CNV)?

Menace and blink reflexes

55

Which muscles test jaw closure?

Temporalis and masseter

56

How is the motor function of CNV tested?

Jaw closure (temporalis and masseter) and jaw opening (pterygoids)

57

Which side will the jaw deviate to if there is a lesion of CNV on the left?

Jaw deviated toward side of lesion (i.e., toward left)

58

When would you see an exaggerated jaw jerk?

In an UMN lesion case

59

What is the function of the facial nerve?

Sensory to ear, muscles of facial expression, stapedius bone, lacrimal gland, salivary glands (except parotid)

60

What 4 functions are tested in examination of the facial nerve?

1. Raise eyebrows 2. Close eyes tightly 3. Show teeth 4. Puff out cheeks

61

Describe the presenation of someone with a right LMN facial palsy

Lower side of face opposite lesion is affected, but upper part of face is not affected

62

What is the function of CNVIII?

Auditory, vestibular (semicircular canals, otoliths)

63

List the 4 tests of CNVIII

1. Crude test of acuity (rub fingers together) 2. Rinne test for conductive defect 3. Weber test of lateralisation 4. Look in the ear

64

In conductive hearing loss, what changes will be observed in the Rinne test?

Air conduction no longer louder than bone conduction (as would be normal)

65

Describe what will be seen in the Weber test of a patient with a sensoneural lesion vs conductive hearing loss

Sensorineural = sound will localise to the opposite side; Conductive loss = sound localises to the same side (normal is equal input from both ears, so sound is heard centrally when fork is placed in midline)

66

What 3 tests are used to assess the vestibular components of CNVIII?

1. Look for nystagmus in 9 cardinal positions of gaze 2. Caolric tests (cold, opposite; warm, same) 3. Lesion = opposite

67

What are the functions of CN IX?

Sensory to ear and fauces. Taste. Motor to stylopharyngeus. Innervates carotid body/sinus, parotid gland and sensory component of gag reflex

68

What are the functions of CN X?

Multiple autonomic, sensory to ear, pharyngeal plexus, soft palate, larynx

69

Which 3 tests are used to test CNX?

Palatal elevtation, cough and motor part of gag reflex

70

Which cranial nerves are responsible for the sensory vs motor component of the gag reflex?

Sensory component via IX (and elicited by gag reflex test), and motor component via CN X

71

In a lesion of the 10th cranial nerve, to which side does the uvula deviate?

Away from the side of the lesion

72

Which physical examination finding could point to a lesion of the vagus nerve on the right side?

Palatal elevation where the uvula deviates away from the side of the lesion (i.e., to the left)

73

What is a bovine cough, and what does it suggest?

Non-explosive cough of a patient who is unable to close his/her glottis. Seen in vagus nerve lesions.

74

How is CN XI tested?

1. Trapezius tested by shrugging 2. Sternomastoid tested by asking patient to turn head against resistance

75

What are the functions of CNXI?

Pharyngeal plexus and trapezius, steromastoid

76

What are the only muscles truly supplied by CNXI?

Constructors of the pharynx (superior, middle and inferior)

77

What is the function of CN XII?

Motor to the tongue

78

How is CNXII tested?

Ask patient to stick tongue out in midline (also observe for abnormalities/fasisculations etc)

79

If there is a CNXII lesion, to which side will the tongue deviate?

To the side of the lesion (because the muscle on that side is now unopposed)

80

What sign on physical examination may suggest a right-sided nerve palsy of CNXII?

Tongue deviating toward lesion (i.e., to the right)

81

Give at least 3 examples of eye movement disorders that are classified by having 'too little movement'

Congenital stabismus, neuromuscular disease, neclear lesions and supranuclear lesions

82

Give at least 2 examples of eye movement disorders that are classified by having 'too much movement'

Saccadic intrusions and nystagmus

83

Malalignment of the eyes can give rise to which symptoms? Name 3

Blurred vision, ghosting, double vision

84

Excess movement of the eyes can give rise to which symptoms? Name 3

Blurred vision, double vision, oscillopsia

85

What is version of the eyes?

Movement of both eyes together

86

What is strabismus?

A misalignment or deviation of the visual axes

87

List at least 2 types of strabismus

Tropia, phoria

88

What is tropia (strabismus)?

Relative deviation of visual axes with both eyes viewing (manifest misalignment)

89

What is phoria (strabismus)?

Relative deviation of visual axes with one eye covered (latent misalignment)

90

What is the other name given to congenital strabismus?

Squint

91

List some causes of congenital strabismus

Defective central vision, impared vision in one eye, anatomic disturbance to the orbit, accommodative discrepancy

92

List at least 3 neuromusclar problems of the eye

CN III nerve palsy, CN IV nerve palsy, CN VI nerve palsy

93

List the 3 degrees of freedom of the eyeball

Horizontal, vertical and tortional

94

What are the actions of the superior oblique occular muscle, if the eye is initial in the primary position?

Depression, intorsion and abduction

95

What are the actions of the superior oblique occular muscle, if the eye is initial in the adducted position?

Pure depression

96

In what position must the eye be in, in order to elicit pure depression of the superior oblique?

Adduction

97

Which occular muscle elevates the eye from the adducted position vs abducted position?

Adducted = inferior oblique; Abducted = superior rectus

98

Which occular muscle depresses the eye from the adducted position vs abducted position?

Adducted = superior oblique; Abducted = inferior rectus

99

Describe the clinical manifestations of a CNIII nerve palsy

Complete ptosis of eyelid and failure of elevation, depression and adduction of eye (due to palsy of SR, IO, IR and MR)

100

What are the 2 divisions of CNIII, and why is this clinically significant?

Superior and inferior - significant because it is possible to get a palsy in only one branch and thus clinical signs will be different

101

What is the superior division of CNIII responsible for?

Superior rectus muscle and levator palpebrae superioris

102

What is the inferior division of CNIII responsible for?

IR, IO, MR and pupil/ciliary body

103

Describe what would be seen in a palsy of only the superior division of CNIII?

Palsy of SR (inabiliy to look up) and levator palpabrae superioris (droopy eyelid), but with preservation of IR, IO, MR and pupil

104

A patient who is tilting their head may have an underlying palsy of which occular cranial nerve?

CN IV (trochlear) > superior oblique

105

In a patient with a CNIV palsy, what will the Bielschowsky head tilt test show?

Eye elevates with head tilt to the side with the CNIV palsy

106

Describe the horizontal gaze pathways

Horizontal eye movements are conducted by the medial rectus and the lateral rectus muscles, which are innervated by the oculomotor nerve (cranial nerve III) and the abducens nerve (cranial nerve VI), respectively. The oculomotor and the abducens nuclei are interconnected by a tract in the brainstem named the medial longitudinal fasciculus (MLF). Through the MLF, the actions of the oculomotor and the abducens nuclei are coordinated, generating conjugate horizontal eye movements.

107

List the 3 disorders of horizontal eye movements

Lateral gaze palsy, internuclear ophthalmoplegia and one-and-a-half- syndrome

108

What is lateral gaze palsy caused by?

Lateral gaze palsy is caused by a lesion involving the abducens nucleus (CNVI)

109

What is internuclear ophthalmoplegia caused by?

Internuclear ophthalmoplegia occurs as a result of a lesion involving the MLF (medial longitudinal fasisculus)

110

What is one-and-a-half syndrome caused by?

Combination of lateral gaze palsy and internuclear ophthalmoplegia caused by a lesion involving both the ipsilateral abducens nucleus (CNVI) and the ipsilateral MLF (medial longitudinal fasisculus)

111

What is lateral gaze palsy?

inability to produce horizontal, conjugate eye movements in one or both directions

112

Discuss the pathophysiology of lateral gaze palsy

Lesions of the cranial nerve VI (abducens) nucleus in the pons cause ipsilateral, horizontal gaze palsy by disrupting motoneurons that innervate the ipsilateral lateral rectus muscle by way of cranial nerve VI, and interneurons that connect to the contralateral cranial nerve III nucleus in the midbrain, via the medial longitudinal fasciculus, to stimulate the medial rectus of the opposite eye

113

What are the 5 types of eye movement?

Vestibular, optokinestic, sacacdic, smooth pursuit and convergence

114

List at least 3 of the inappropriate saccades seen in eye disorders

1. Square wave jerks 2. Macro square wave jerks 3. Flutter 4. Opsoclonus 5. Voluntary nystagmus

115

What are the 2 physiological types of nystagmus?

1. Physiological nystagmus 2. Pathological nystagmus

116

What are the 2 types of physiological nystagmus?

Vestibular nystagmus and optokinetic nystagmus

117

List the 3 common types of pathological nystagmus

1. Vestibular 2. Cerebellar/brainstem 3. Congenital

118

List 2 different rhythms seen in nystagmus

Pendular, jerk

119

Pure vertical nystagmus in primary position implies what sort of cause?

Central

120

What sort nystagmus is unaffected by posture, better on convergence or lid closure but worse with fixation, attention and anxiety?

Congenital nystagmus

121

What is learning?

Process of acquiring new information and results in an observable change in behaviour

122

What is memory?

The encoding, storage and retrieval of learned information

123

List some types of molecular memory

1. DNA, RNA 2. Epigenetic tage on DNA 3. Changes in transcription (programs) 4. Conformational changes of protein (prion) 5. Protein modification 6. Changes in intracellualr signalling cascades

124

List some types of neuronal memory

Synaptic plasticity, changes in intracellular signalling cascades (kinases, phosphatases), structural changes (growth of dendrites or pruning), changes in excitability, consolidation of memory to achieve storage

125

What is delarative memory? Give some examples

Items available to consciousness and can be expressed by language ('declare'): phone number, song, images of previous events

126

What is nondeclarative memory? Give some examples

Items not directly available to consciousness: skills (skiing), associations, priming cues etc. Difficult ot express how procedures are enacted.

127

What are the 2 major categories of memory?

Declarative and non-declarative

128

What are the 3 types of delarative memory?

Daily episodes, words and meanings, history

129

What are the 4 types of non-declarative memory?

Motor skillls, associations, priming cues and puzzle-solving skills

130

What are the temoral categories of memory?

Immediate memory (retention of experiences for less than 1 second) ; Working memory (holding of experience to achieve behavioural goal - seconds - minutes); Lon-term memory (days to years) - long-term retention - requires transfer from working memory to memory via consolidation

131

What sort of memories are forgotten fastest?

Those of no particular importance (short-term)

132

What sort of memories deteriorate over time?

Unused memories (normal process)

133

What is anterograde amnesia?

Inability to create new memories

134

What is retrograde amnesia?

Inability to retrieve made memories

135

List the 2 types of pathalogical amnesia

1. Anterograde 2. Retrograde

136

Anterograde amnesia affects what type of memory?

Declarative memory

137

Explain why someone with anterograde amnesia may not remember daily life, words and history, but may be able to learn new motor skills?

Because anterograde amnesia primarily is associated with loss of delarative memory, but not non-declarative memory.

138

Vascular occlusion of both posterior cerebral arteries causes damage to which sites that can lead to anterograde amnesia?

Bilateral medial temporal lobe and hippocampus (CA1)

139

Midline tumours can cause damage to which sites that can lead to anterograde amnesia?

Medial thalamus bilaterally (may involve hippocampus is large enough)

140

There is a tight correlation between ____ damage and anterograde amnedia

Hippocampal (medial temporal lobe)

141

What functions of the hippocampus are destroyed as a result of damage to the medial temporal lobe?

Formation of memory and processing for consolidation (but not memory storage, as hippocampus not responsible for this)

142

Trauma, surgery and infections can cause damage to which speicifc site that can lead to anterograde amnesia?

Bilateral medial temporal lobe

143

Vitamine B deficiency can cause damage to which specific sites that can lead to anterograde amnesia?

Medial thalamus and mammillary bodies

144

Discuss the brain changes seen in taxi drivers

Larger posterior hippocampal volume (as hippocampus is an encoder and temporary buffer for short-term and working memory)

145

Which 2 brain areas are considered to be systems for declarative memory?

Hippocampus and parahippocampal gyrus

146

Discuss the input and output of the hippocampus as a system for declarative memory

Widespread projections from association neocortex converge on the hippocampus. The output is ultimately directed back to the same neocortical areas.

147

What abnormality occurs in Wernicke's aphasia of the superior temporal lobe?

Inability to link sound with meaning of word

148

What abnormality of memory occurs in patients with temporal lobe lesions?

Inability of recognise objects and/or faces

149

What lobe is involved in the attempt to retrieve long term memories?

Frontal

150

What part of the brain is specifically activated when recalling vivid memories?

Visual association cortex

151

List the 5 areas of the brain involved in non-declarative memory

1. Basal ganglia 2. Prefrontal cortex 3. Cerebellum 4. Amygdala 5. Somatosensory cortex

152

Give an example of an action which proves that there are more integrative systems involved in non-delarative compared to declarative memory

Perceptual priming, eye blinke etc.

153

Decrease in learning task performance in Parkinson's disease is improved with the use of which NT drug?

L-DOPA

154

Which pathway of the basal gangalia is of special importance to motor skill learning?

Prefrontal cortex loop

155

Which NT is involved in memory formation of motor skill learning?

L-DOPA

156

Sleep improves what type of memory?

Nondeclarative

157

Improved consolidation of nondeclarative memory/learning in sleep is tightly correlated with what sleep stage at what time of night?

NREM stage 2 (deep sleep) in the fourth quarter (towards morning)

158

The conversion of short-term to long-term declarative memory relied on what specific function?

NREM sleep

159

Short term declarative memory is sotred in what area?

Hippocampus and related structures

160

Short term non-declarative memory is sotred in what area?

Unknown, but presumably widespread

161

Long term declarative memory is offloaded from the hippocampus and stored in what cortical areas?

Variety of cortical areas: Wernicke's area (words), temporal cortex for objects, faces etc.

162

Long term non-delarative memory is stored in what area?

Cerebellum, basal ganglia, premotor cortex, and other sites related to motor behaviour

163

What is synaptic plasticity?

Changes in synaptic efficacy, including postysynaptic excitability and spine/cellular growth

164

In relation to the cellular basis of memory, what is the name given to synapses that become stronger with time? What is the opposite?

Long-term potentiation; long-term depression

165

List the 4 changes observed as a result of tetanic stimulation of PP (perforin path)

Population spike increase, increase in excitability, increased field EPSP (reflection of synaptic currents) and increased synaptic currents

166

Tetanic stimulation of PP (perforin path) causes changes that last for how long?

over 12 hours - up to months

167

List and describe the 3 properties of long-term potentiation

1. Input specific - only stimulated synapses potentiate 2. Associativity: when a weak input is sufficient for induction, strong stimulation of another input induces LTP at both inputs 3. Cooperatively - several small inputs each insufficient for induction, when stimulated together induce a LTP

168

What occurs in the induction phase of long-term potentiation?

Immediate postsynaptic calcium rise; mostly via NMDA receptors

169

What occurs in the expression phase of long-term potentiation?

Calcium activated; insertion and phosphorylation of AMPA receptors causing larger post-synaptic current and altering receptor cycling > main effect is increase in excitability

170

What occurs in the maintenance phase of long-term potentiation?

Autoactivation of CaMK II - protein synthesis is activated and there is growth of new excitatory synapses; gene expression is altered (CREB)

171

Which 3 factors improve memory formation?

1. Association 2. Motivation 3. Forgetting

172

Declarative memories rely on the _____ as a buffer, and on the ____ as final storage

Hippocampus; cortex

173

Non-declarative memories rely on specifiv areas of the brain typically involved in what functions?

Motor control and coordination

174

Long term potentiation is induced ____synaptically via ____ ions via ____ receptor

Post; calcium; NMDA

175

How is long term potentiation maintained?

Via altered gene expression and protein synthesis

176

The caudate nucleus is located next to which brain structures?

Latreal walls in lateral ventricles

177

What are cortico-striatal circuits?

Neural networks that allow organisms to interact adaptively with their environments

178

Which 2 main components make up neural networks in the brain?

Hubs (nuclei, cortical loci) and spokes (white matter neural connections)

179

List the 5 cortico-striatal circuits

1 Orbitofrontal circuit 2. Anterior cingulate circuit 3. Occulomotor circuit 4. Dorsolateral prefrontal circuit 5. Supplementary motor circuit

180

The cortico-cerebellar pathway exists between which major structures?

Cerebellum, cortex, pons, thalamus

181

Which 2 cortico-striatal circuits regulate motor functions? What are the other functions of these pathways?

SMC and OMC - influence skeletomotor and oculomotor areas of the cortex

182

Which 3 cortico-striatal circuits regulate non motor areas of the prefrontal cortex?

ACC, OFC and DLPFC

183

Discuss the origin, projection and clinical manifestations related to the orbitofrontal circuit

Originates in orbitofrontal regions; projects to the ventromedial caudate nucleus; clinical manifestations are characterised by deficits in social judgement and impulse control

184

Discuss the origin, projection and clinical manifestations related to the anterior cingulate circuit

Originates in anterior cingulate gyrus; projects to ventral striatum (nucleus accumbens); clinical menifestations are apathy, akinetic mutism and are characterised by lack of motivation

185

Damage to which cortico-striatal circuit may cause deficits in social judgement and impulse motor control?

Orbitofrontal

186

Damage to which cortico-striatal circuit may cause apathy, akinetic mutism and lack of motivation?

Anterior cingulate circuit

187

Discuss the origin, projection and clinical manifestations related to the oculomotor circuit

Originates at the FEF and posterior parietal cortex; projects to the body of the caudate nucleus; clinical menifestations include visuospatial dysfunction and visual apraxia

188

Damage to which cortico-striatal circuit may cause visuospatial dysfunction and visual apraxia?

Oculomotor circuit

189

Where does the dorsolateral prefrontal circuit originate and project to?

Originates at the dorsolateral surface of the anterior frontal lobe; projects to dorsolateral had of the caudate nucleus

190

What are the functional roles of the dorsolateral prefrontal circuit?

Regulate executive function - anticipation, goal selection, planning, use of feedback in task performance, cognitive flexibility

191

Where does the supplementary motor circuit originate and project to?

Originates at the supplementary motor, premotor and motor cortices; Projects to the putamen

192

What are the functional roles of the supplementary motor circuit?

Planning and execution of movement as well as regulating overall amount, scale and focus of movement

193

Huntington's disease is a ____ change in cortico-striatal circuits, whereas Parkinson's disease is a _____ change

Structural; functional

194

Huntington's disease primarily affects the _____, whereas Parkinson's affects the ______ (both basal ganglia structures)

Caudate; putamen

195

What is the inheritence pattern of Huntington's disease?

Autosomal dominant

196

What is the best known disorder affecting primarily the caudate nuclei (although atrophy becomes widespread with disease progression

Huntington's Disease

197

Describe some of the gross changes in the brain of a patient with Huntington's disease

Dlation of lateral ventricles and atrophy/death of caudate

198

Compare the motor changes seen in Pre-Huntington's disease vs Huntington's disease

Minor deficits in more complicated tasks vs chorea +/- tics, gait disturbance, incoorination, eye movement disorders

199

Compare the cognitive changes seen in Pre-Huntington's disease vs Huntington's disease

Executive dysfunction, mild impairment and slower processing speeds vs HD dementia

200

Compare the psychiatric changes seen in Pre-Huntington's disease vs Huntington's disease

Anxiety, paranoid ideation, psychotic elements vs disibhibition, apathy, depression, anxiety, delusional disorder, psychosis, suicidal behaviour

201

Huntington's disease disrupts the ______ ______ circuit by damaging the _____ ____ node

dorsolateral prefrontal circuit; caudate nucleus node

202

Cognitive deficity in huntington's disease reflect involvement of what basal ganglia structure?

Head of caudate nucleus

203

Which proteins fold abnormally and become neurotoxic in Parkinson's disease?

Alpha-synuclein

204

At diagnosis of Parkinson's, what % of cell death has already occurred?

70%

205

What are the motor manifestations of Parkinson's disease?

Akinesia, bradykinesia, tremor, rigidity, postural instability

206

What are the neuropsychiatric manifestations of Parkinson's disease?

Autonomic, REM sleep behaviour, hyposmia, cognitive, depression, demantia

207

Parkinson's disease disrupts the ____ _____ circuit due to loss of dopaminergic input to _____ node

Supplementary motor; putamen

208

Insufficient dopamine at the putamen has what effect on the motor cortex? What physical signs correlate with this?

Increased thalamic inhibition of motor cortex = rigidity and bradykinesia

209

How can deep brain stimulation work as a treatment for parkinson's disease?

DBS mimics a lesion using electrical implants and pacemaker > can be used to minimise abnormal neuronal drive of subthalamic nucleus, globus pallidus internus and thalamus > restores the functioning of the supplementary motor circuit by reducing inhibition of thalamus over motor cortex > enables voluntary movement and reduces rigidity

210

The cortex of the cerebellym consists of how many layers?

3 layered sheet of organised cells and fibres

211

Describe the cortico-cerebellar circuit that connects the cerebellum to the prefrontal regions

Cerebellum > ventral dentate nucleus > thalamus > prefrontal cortex > pontine nucleus closes the loop to the cerebellum again

212

Describe the cortico-cerebellar circuit that connects the cerebellum to the motor regions

Cerebellum > dorsal dentate nucleus > thalamus > motor regions > pontine nucleus closes the gap to the cerebellum again

213

What is the purpose of cortico-cerebellar circuits and motor inolvement?

Circuits connected to motor regions enable integration of separate movements into a coordinated whole

214

What is the purpose of cortico-cerebellar circuits and congnitive inolvement?

Circuits connected to prefrontal regions conduct automatic information processes, leaving the prefrontal cortex free to solve new cognitive problems

215

List 5 manifestations of cerebellar ataxias

Gait/posture: instability, balance issues, falling and tripping; Fine motor incoordiantion: difficulty handwriting, cutting food, buttoning; Speech: slurred and slow (agrammatism); Cognitive: impaired memory, incorporating information, kaing plans and ordering thoughts; Mood: increased irritability, anxiety and depression

216

What factors are needed to establish a diagnosis of inherited cerebellar ataxia?

Detection of symptoms, positive FHx of ataxia, causatative allelic variant to a gene associated with hereditary ataxia, clinical phenotype characteristic of a genetic form of ataxia

217

Executive motor movements are under the direction of which brain areas?

Area 6 (primary motor cortex) and basal ganglia

218

What is area 6 of the brain responsible for?

Skilled voluntary motor movements

219

The secondary motor area innervates which muscle group directly?

Distal muscle groups

220

The premotor area of the brain connectes with _____ neurons to innervate _____ motor units

Reticulospinal neurona; proximal motor units

221

Which area of the brain is involved in the design of movements?

Premotor area

222

Where does the neostriatum get inputs from?

Cortex and substantia nigra pars compacta

223

Where is the subthalamic nucleus located?

Below the thalamus and above the hypothalamus

224

What is the net effect on motor activity from the direct basal ganglia pathway?

Increases motor activity

225

What is the net effect on motor activity from the indirect basal ganglia pathway?

Decreases motor activity

226

What signs must be absent in order to diagnose a movement disorder?

Absence of spacticity (i.e., not involving corticospinal tracts), absense of weakenss and decreased coordination

227

Movement disorders are a groups of neurological conditions which exhibit which 2 major features?

1. Paucity of movement (brady/hypo/a-kinesia) 2. Excess of abnormal involantry movement

228

What causes the signs seen in movement disorders?

Increased muscle contractions and motor inhibitions (asterixis, cataplexy)

229

List at least 4 types of bradykinetic movement diroders

Parkinsonism, catatonia (psychomotor depression), neuroleptic malignant syndrome, gait freezing (gait apraxia), stiffperson syndrome and cataplexy

230

Which system of the brain is mostly affected in Parkinsons?

Extra pyramidal

231

List the 4 cardinal features that assist in the diagnosis of Parkinsons disease

1. Tremor 2. Rigidity/stiffness 3. Slow movement (bradykinesia) 4. Loss of balance (postural instability)

232

List at least 5 red flags for minics of Parkinsons' disease

Absence of tremor, symmetrical onset, rapid progression, cognitive decline, pyramidal signs and dysautonomia

233

List the areas affected by loss of dopamine producting cells in Parkinsons

Substantia nigra, bain stem, olfactor tract and gut

234

At what % of cell loss does Parkinson's disease cbbecome symptomatic?

60-80%

235

Lewy body formation is seen in which neurodegenerative disorder?

Parkinsons

236

Dopamine deplation in Parkinsons causes issues in which 3 major areas?

1. Motor 2. Automonic 3. Cognition

237

List at least 3 anti-Parkinson medications

Levodopa, dopamine agonists, MAO type B inhibitors, COMT inhibitors, amantadine

238

What is stiff person syndrome?

Muscle rigidity and spasm involving axial and limb muscles (possibly autoimmune against GABA transmission)

239

List at least the 4 diagnostic criteria for stiff person syndrome

1. Insidious onset of muscular rigidity with difficulty turning or bending, most prominent in limbs/axial muscles (esp abdo and thoracolumbar) 2. Co-contraction of agonist and antagonist muscles, confrimed clinically and electrophysiologically 3. Episodic spasms superimposed on the underlying rigidity, precipitated by noise, tcile stimuli or emoton upset 4. Absence of other neurologic or systmic disease to explain the symptoms

240

List the clinical findings of a patient with stiff person syndrome

Rock hard muscles in symptomatic regions, hyperlordosis, paraspinal muscle spasm, stiff gait, stiffness of a single limb, sustained clonus, hyperreflexia, cerebellar syndrome and cock-up toe

241

Give an example of an immunomodulator drug that may be used to treat a patient with stiff persons syndrome

Predisoone, methylprednisolone, IVIG, plasma exchange

242

Give an example of an immunosuppresant drug that may be used to treat a patient with stiff persons syndrome

Cyclophosphamide, azathioprine, rituximab

243

Give an example of synptom-control drug that may be used to treat a patient with stiff persons syndrome

Baclofen, clonazepam, levodopa

244

What is the tetrad of neuroleptc malignant syndrome?

1. Altered mental status 2. Muscle rigiditiy 3. Fever over 38 degrees 4. Autonomic instability

245

Discuss the pathophysiology of neuroleptic malignant syndrome

Inhibition of central dopamine receptors in hypothalamus - causing increased heat generation and decreased heat dissipation

246

What sort of drugs may cause neuroleptic malignant syndrome?

Typical antipsychotics or sudden withdrawal of L-Dopa

247

Which blood chemistry marker correlates with increased severity of neuroleptic malignant syndrome?

Creatinine Kinase

248

Discuss the abnormalities seen in investigations for neuroleptic malignant syndrome

Elevated CK, leucocytosis, mildly elevated LDH, ALP and transaminases, increase potassium and/or decreased magnesium

249

What is the treatment for neuoleptic malignant syndrome?

Stop the offending drug, give a muscle relaxant and supportive therapy (such as antipyretics).

250

List 3 signs to watch for when treating a patient for neuroleptic malignant syndrome

Dehydration, ARF with rhabdomyolysis, arrythmis respiratory failure, DVT and seizures

251

The initial therapy for parkinsons disease depends on which patient factor?

Age

252

List some of the symptoms in late parkinsons disease

Non-motor symptoms and motor fluctuations

253

What are some of the treatment options for late parkinsons?

Apomorphine, duodopa, DBS

254

50-60% of patients with stiff persons syndrome have which marker in the serum and CSF?

Anti-GAD

255

Give at least 3 examples of hyperkinetic rhythmic movements

Tremor, myoclonus, myorhythmia, dystonic tremor, periodic movements in sleep

256

Give at least 3 examples of hyperkinetic irregular movements

Tics, chorea, athetosis, dystonia, ballism, hemifacial spasm

257

What is the definition of tremor?

Involuntary rhythmic, repetitive, oscillatory movement of a body part around a central joint caused by alternate contraction of agonist and antagnosit muscles

258

What sort of drugs can be used for essential tremors?

Beta blockers, primidone, clonezapam

259

What sort of surgery may be used to stop essential tremors?

DBS of thalamus

260

What is the definition of myoclonus/startle?

Sudden brief, shock-like jerky movements of limb/axial muscles

261

What is restless leg syndrome?

Unpleasant sensation in legs with irresistable desire to move (which provides relief) especially when lying down and mostly when about to sleep.

262

What may be used in the treatment of restless leg syndrome?

L-Dopa, DA

263

List some of the disorders that restless leg syndrome is associated with

Hereditary, neuropathy, uraemia, iron deficiency, pregnancy hypothyroidism

264

What is the definition of tics?

Brief, quick, coordinated, intermittently repetitive movements or sounds of a single muscle group - able to be suppressed

265

What are the 4 clinical type of tics?

1. Simple motor 2. Complex motor (purposeful) 3. Simple phonic 4. Complex phonic (linguistic)

266

List 1 drug that may be used to treat tics?

Clonezapam

267

Define chorea

Involuntary, irregular unsustained movements, purposeless and non-rhymic in nature

268

List some of the primary and secondary causes of chorea

Primary = huntingtons, benign hereditary chorea, neuroacanthocytosis; Secondary = Sydenhams chorea, immune mediated SLE, infecious chorea and from drug use

269

What is ballism?

Proximal, flinging random movements that are usually unilateral and improve spontaneously

270

What is athetosis?

Writhing, random, slow chorea induced by voluntary movements

271

What is the definition of dystonia?

A syndrome of sustained/intermittent contraction of voluntary muscles frequently causing twisting and repetitive movement or tremor/abnormal postures sometimes associated with pain

272

List at least 3 pharmacological treatments for dystonia

Anticholinergics, antiepileptics, antidopaminergics, muscle relaxants, target-specific (botox)

273

Describe the mechanism of action of botulinum toxin

Once inside cell, blocks release of ACh transmitter. This results in chemo-denervation

274

What is a hemifacial spasm?

Unilateral, involuntary contraction of one side of the face. Chronic and progressive caused by compression of the facial nerve by arteriole.

275

What is hemifacial spasm often misdiagnosed as?

Epilepsia partalis continua

276

Describe the different clinical signs observed in abductor vs adductor types of laryngeal dystonia

Abductor type = whispering voice; Adductor type = strangled sound (spasmodic dysphonia)

277

Huntington's disease is an inherited form of ____

Chorea

278

Drug-induced movement disorders are commonly due to which class of drug?

Antipsychotic agents

279

What age groups of men and women are most commonly affected by gout?

Men over 40 and women over 55 (male prevalence 5:1)

280

List at least 5 risk factors for gout

Hyperuricaemia, obesity, high-prurine diet (red meat), alcohol, high fructose drinks, medications (thiazide diuretics or cyclosporin), renal insufficiency, lead exposure, organ transplantaion, hypertension, diabetes, hyperipidaemia etc.

281

List at least 3 explanations for why there is an increased prevalence of gout in the elderly

Longevity of population, increased prevalence of vascular disease, increased use of diuretics, immunosuppressive therapies, renal disease and transplants, obesity and associated metabilic syndrome, dietary trends

282

What is the link between cardiovascular disease and gout?

Both gout and CVD are associated with serum markers of inflammation - CVD risk is increased in people with gout or hyperuricaemia

283

Uric acid is the end product of what metabolic process?

Purine metabolism

284

Uric acid is present in the serum and tissues in what form?

Monosodium urate

285

At what point do uric acid levels supersaturate the serum and precipitate into tissues?

0.4mmol/L monosodium urate

286

Discuss the basic process that leads to gout

When serum uric acid (monosodium urate) levels rise too high (above 0.4mmol/L), it supersaturates the serum and precipitates into tissues. An acute gouty attack occurs when monosodium urate crystals are released or form de novo in joint spaces. Crystals induce inflammation and phagocytosis by neutrophils (plus the release of Iinflammatory mediators)

287

List at least 2 medications that can abruptly alter uric acid levels and incite an attack of gout

llopurinol, diuretics

288

Aside from drugs, what other factors can rapidly change uric acid levels and incite a gout attack?

Trauma, surgery, infections

289

Discuss the pathophysiology of gout

Serum urate rises and becomes supersaturated > precipitates into tissues, forming monosodium urate crystals > crystals phagocytosed by leucocytes > once inside cell, crystals trigger inflammatory reaction which is mediated by a group of inflammasome proteins > inflammasome potentiates IL-1 converting enzyme, which formed active IL-1 beta > further release of inflammatory cytokines, prostaglandings and vasoactive pepties and local amplification of the process occurs

290

What is the inflammasome?

A multi-proteins cytoplasmic complex that activates cascades and leads to the processing and secretion of proinflammatory cytokines such as IL-1beta

291

What mediates inflammasome assembly?

NOD-like receptor protein family members that carry an N-terminal pyrin domain (NLRPs) or a capsase-recruitment domain (NLRCs)

292

NLRP3 (nod-like receptor with N-terminal pyrin domain) can be activated by what molecular patterns?

Pathogen-assocated (PAMPS) and damage associated (DAMPS)

293

List the 2 main types of acute gout

Mono-articular, oligo or polyarticular

294

List a type of chronic or interval gout

Tophaceous gout

295

What are the initial investigations for asumptomatic hyperuricaemia?

Fasting lipid profile and BSL and 24 hour urine UA

296

What are the initial investigations for symptomatic gout?

FBC, CRP, blood cultures, serum uric acid, EUC, LFT, fasting lipi profile and BSL. Synovial fluid for gram stain, cells, culture and crystals

297

What is the gold standard for diagnosing gout?

Demonstration of MSU (monosodium urate) crystals

298

Discuss the usefulness of US and MRI in gout investigation

Useful when there is a presence of tophii and larger crystal deposits, but no overall improvement in diagnostic sensitivity or specificity

299

What are the main differential diagnoses for gout?

Rheumatoid arthritis and pseudogout (calcium phosphate deposition disease), septic arthritis, cellulitis, reactive arthritis, ostoarthritis, psoriatic arthritis, sacoidosis

300

List some of the signs that favour a diagnosis of RA over gout

In RA: symmetrical polyarthritis of small joints common, hand involvement more likley, subcutaneous nodules may be present, imagine will show soft tissue welling, diffuse joint-space narrowing, marginal erosions of small joints

301

List some of the signs that favour a diagnosis of pseudogout over gout

In pseudogout: appears in unusual places like the wrist or elbow without trauma, loows like RA or osteoarthritis on imaging but shoes signs of repair, there is cartilage calcification

302

List some of the signs that favour a diagnosis of septic arthritis over gout

Septic arthritis: fever, great tenderness, joint sepsis may be present, may have concommitant rheumatoid arthritis, source often evident, imaging shows swelling and effusion

303

List some of the signs that favour a diagnosis of cellulitis over gout

In cellulitis: erythema, swelling of extremity, very tender, often febrile, sodt tissue lymphatic drainage abnormal due to peripheral venous insufficiency, soft tissue swelling on imaging

304

Cellulitis is often due to infection by which pathogens?

Staph or strep

305

List some of the signs that favour a diagnosis of reactive arthritis over gout

In reactive arthritis: soft tissue swelling, oligoarthritis, weight bearing joints affected at tendon insertions, dactylitis may cause digits to resemble sausages, depending on infecting pathogen, may also see other signs of infection like skin changes, conjunctivitis etc.

306

List some of the signs that favour a diagnosis of OA over gout

Bony enlargement without acute inflammation, exacterbation of joint symptoms after use, imging shows focal joint space loss, bony repaire with osteophytes and subchrondral sclerosis, central erosions may be present in finger joints and often involves bunions (which is also common in gout)

307

What is halus valgus?

Bunion

308

Compare and contrast MSU crystals vs CPPD crystals

CPPDs are rhomboid or rectangular and have positive birefringence, but less so than MSU (appear blue). MSU crystals are brghtly birefringement and needle shaped and appear yellow.

309

If suspecting gout and synovial fluid analysis comes back negative for crystals, what could have happened?

Delay in examining unrefrigerated fluids

310

Why is hyperuricaemia (even when asymptomatic) clinically relevant?

Due to urate-related associations with hypertension, insulin resistance and CVD > therefore require screening and lifestyle modification

311

Discuss the recommended primary prevention of gout

Dietary modification and weight loss to reduce risk factors and lower serum urate levels. Pharmacologic therapy only recommended in patients on chemotherapy for haematologic malignant conditions

312

Discuss why pharmacologic therapy is recommended as primary gout prevention in patients on chemotherapy for a haematologic malignant condition

Uric-acid lowering drugs and hydration prevent secondary group due to tumour lysis. Without this treatment, uric acid neuropathy with tubular obstruction can develop

313

List the symptoms and physical examination findings that suggest gout

Warmth, swelling, redness, severe and episodic self-limiting joint pain, attacks at night or early morning

314

Acute gout attacks usually subside in what time period?

3-14 days without treatment

315

What are the common sites for crystal deposition/tophus deposition in gout?

Helix of the ear, lower extremities

316

List some of the risk factors that increase the liklihood of progression fro asymptomatic hyperuricaemia to gout

Renal impairement, lymphoproliferative or myeloproliferative disorders, psoriasis, vitamin B12 deficiency, current chemotherapy for blood malignancy

317

What is the long term aim for the management of gout?

Reduce serum uric acid levels to below 0.36mmol/L

318

What are the general indications for urate-lowering treatment in gout?

Recurrent attacks, chronic tophaceous gout, presence of changes on imaging, coexisting nephrolithiasis, renal insufficiency, presence of metabolic syndrome and coexisting gout with diuretic therapy

319

What sort of diet should be recommended in patients with gout?

Decrease high-purine foods, reduce alcohol and surgary drinks, lots of water, high fibre, high vit C, high folate

320

List some high-purine foods

Red meat, seafood, yeast products like baked goods, mushrooms, spinach, asparagus, cauliflower, legumes

321

List the 3 broad classes of anti-gout drugs and state how each works

1. Xanthine oxidase inhibitors (reduce production of serum uric acid) 2. Uricase enzyme analogues (reduce SUA by converting to allantoin) 3. Uricosuric agents (increase UA excretion)

322

Which drugs are first-line for treating acute gout?

NSAIDs - due to anti-inflammatory and analgesic effects

323

What is pseudogout?

A crystal arthropathy associated with ageing, where there is acute arthritis with characteristic calcifications in cartilage (chondrocalcinosis) and calcium pyrophosphate dihydrate (CPPD) crustals in synovial fluid

324

What is the calcification of cartilage called (as in pseudogout)?

Chonrocalcinosis

325

Which joints are commonly involved in pseudogout?

Knees, wrists, shoulder, hips and ankles

326

Pseudogout has greatest prevalence in which age group?

Over 85 years

327

What is essential in the diagnosis of pseudogout?

Demonstration of crystals in synovial fluid analysis (supported by radiographic cartilage calcification)

328

What disorder should be expected when radiological features of OA are evidence in joints not commonly affected in primary OA?

CPPD crystal deposition disease (i.e., pseudogout)

329

List the 4 radiological features of gout

1. Erosions with overhanging margins 2. Sclerotic margins 3. Relatively well-preserved joint spaces 4. Soft tissue tophi

330

List the 3 major functions of the cerebellum

1. Maintain synergy of movement (coordination) 2. Maintain upright posture (and maintenance of balance) 3. Monitor and maintain muscle tone

331

List 3 functions that the cerebellum specifically monitors and adjusts

1. Contraction and relaxation of oppponent muscle groups 2. Intensity and duration of muscle contractions 3. Sequencing of contractions of muscle groups required to execute a specific movement

332

The cerebellum gets input from the motor cortex via which 2 pathways?

Cortico-pontine and ponto-cerebellar

333

The cerebellum gets feedback from the peripheral muscles via which pathway? What sort of information is this?

Proprioceptive information via spino-cerebellar tracts

334

The cerebellum feeds back to the control centres and brainstenabout muscle adjustments via which cortical structure?

Thalamus

335

Name and describe the 3 lobes of the cerebellar cortex

1. Anterior lobe (most of the superior surface) 2. Posterior lobe (most of the inferior surface) and 3. Flocculonodular lobe (discrete region at the anterior inferior surface

336

Which fissure separated the anteiror and posterior lobes of the cerebellum?

Primary fissure

337

Which fissures separates the posterior and flocculonodular lobes of the cerebellum?

Posterolateral fissure

338

List the important functional units that make up the pons

Pontine nuclei + corticospinal tracts + ponto-cerebellar fibres (middle cerebellar pedundle)

339

The ponto-cerebellar fibres pass from the pons to the cerebellum via which peduncle?

Middle cerebellar

340

List the 4 deep nuclei of the cerebellum

1. Dentate 2 & 3. Globose and Emboliform (collectively known as the interposed nulceus) 4. Fastigial

341

Which is the largest deep nuclei in the cerebellum?

Dentate

342

Which deep nuclei of the cerebellum feeds back to motor cortical areas?

Dentate

343

The globose and embolifm nuclei of the cerebellum are collectively known as which nucleus?

Interposed nucleus

344

Describe the location of the deep fastigial nuclei in the cerebellum

Adjacent to midline, sandwhiched between midline and interposed nucleus

345

The interposed nucleus of the cerebellum is associated with what function?

Spino-cerebellar feedback

346

The fastigial nuclei of the cerebellum have functions associated with what system?

Vestibular system

347

All inputs to the cerebellum terminate at what point?

In the cerebellar cortex

348

The cerebellar corte projects to which structures?

Deep cerebellar nuclei

349

All output from the cerebellum originates from which structures?

Deep cerebellar nuclei

350

Deep nuclei outputs in the cerebellum go to which areas?

Thalamus and brainstem nuclei

351

Describe the pathway that originates from the cortex (or pons) and travells through the cerebellum (include what part of the cerebellum the input is to, nucleus and output)

Input > cerebro-cerebellum > dentate nucleus > to UMNs in premotor cortex

352

Describe the pathway that originates from the spinal cord and travells through the cerebellum (include what part of the cerebellum the input is to, nucleus and output)

Input from spinal cord > spino-cerebellum > interposed nuclei > outputs to UMNs in the motor cortex and brainstem

353

Describe the pathway that originates from the vestibular and motor eye cortices and travells through the cerebellum (include what part of the cerebellum the input is to, nucleus and output)

Input > vestibulo-cerebellum > fastigial nuclei > output through vetibular nuclei to LMNs in the medial ventral horn of the spinal cord

354

What information is provided to the cerebellum via the middle cerebellar peduncle (from cortex via pons)?

Informs cerebellum of plan/intention of movement

355

The cerebellum receives information from the spinal cord via which structure?

Inferior cerebellar peduncle

356

Name the 5 sets of fibres with input ot the cerebellar cortex

1. Ponto-cerebellar 2. Reticulo-cerebellar 3. vestibulo-cerebellar 4. spino- and cuneo-cerebellar 5. olivo-cerebellar

357

Outputs to from the cerebellum are sent to the cortex via the _____, with collaterals sent to the ____ _____ and _____ nucleus

Thalamus; superior colliculus; red nucleus

358

What are the afferents of the superior cerebellar peduncles?

Ventral spinocerebellar tract (from mechanireceptors in the trunk and lower limbs)

359

List the 2 output nuclei for efferent information from the superior cerebellar peduncle, along with the primary and secondary target from each nuclei

1. Dentate nuclei > VL thalamus > red nucleus 2. Globose/embomiform nucleus > red nucleus > VL thalamus

360

Cerebellar terminals in the thalamus map co-register with the terminals of which basal ganglia structure?

Globus pallidus internus

361

Which is the only cerebellar peduncle to carry ONLY afferent information?

Middle cerebellar peduncle

362

Decribe the pathway of afferent inputs of the middle cerebellar peduncle?

Cell throughout cerebral cortex send axons through the medial and lateral third of te peduncles > these synapse in pontine nuclei > ponto-cerebellar fibres then cross the midline and enter the cerebellum via MCP and terminate in the cerebellar cortex

363

What are the afferents of the inferior cerebellar peduncles?

Dorsal spino-cerebellar tract fibres and cuneo-cerebellar tracts (also carries inputs from inferior olivary nucleus, vestibular nuclei and brainstem reticular formation)

364

What are the efferent of the inferior cerebellar peduncles?

Fastigial nucleus sends axons to terminate in the brainstem vestibular nuclei

365

Dorsal spino-cerebellar tract fibres originate from cells in what structure? What information do these carry?

Clarke's column (C8-L3); get proprioceptive input from lower limbs and lower trunk

366

The dorsal spino-cerebellar tract fibres terminate in what part of the cerebellum?

Cortex of the anterior lobe

367

The cuneo-cerebellar tract fibres terminate in what part of the cerebellum?

Cortex of the anterior lobe

368

Cuneo-cerebellar tract fibres originate from cells inw hat structure? What information do these carry?

Accessory cuneate nucleus which get input from proprioceptive fibres in levels above C6

369

The inferior olivary nucleus facilitates what function?

Motor learning

370

The inferior olivary nucleus gets descending input from which nucleus?

Red

371

Where does the inferior olivary nucleus send axons to?

C/L cerebellar cortex of the anterior and posterior lobes (olivocerebellar fibres)

372

The olivo-cerebellar fibres comprise a specific input to the cerebellar cortex known as _____ fibres

Climbing

373

What do the climbing fibres of the inferior olivary nucleus do?

Fine tune motor response, especially during learning

374

What are the 2 sorts of fibre inputs into the cerebellum?

Climbing fibres and mossy fibres

375

Climbing fibres that provide input to the cerebellum have their cell bodies in which nucleus? Where do thes efibres receive input from?

Inferior olivary nucleus; input from cerebral motor cortex and cerebellum via red nucleus

376

What is believed to be the function of the climbing fibres supplying the cerebellum? When are they most active?

Encoding of sensory input independently of attention or awareness; most active during learning/training

377

Climbing fibres excite one ______ cell, whilst mossy fibres excite many _______ cells, which in turn activate many _____ cells

Purkinje; granulate cells; Purkinje cells

378

List the 5 typical cell types of the intrinsic cerebellar circuitry

Purkinje, granule, asket, stellate and golgi

379

What do granule cells in the cerebellum do?

Connect many Purkinje and climbing fibres, thereby functionally connecting adjacent structures of the body represented in the cerebellum

380

Which cells of the intrinsic cerebellar circuitry form parallel fibres? What is the advantage of this?

Granule cells; each parallel fibre contacts tens of thousands of Purkinje cells

381

What is the orientation of Purkinje cells in the cerebellum? What is the advantage of this arrangement?

Dendrites oriented perpendicular to parallel fibres of granule cells; can contact 200,000 parallel fibres

382

Purkinje cells impose _____ input to deep nuclei of the cerebellum via ____ neurones

Inhibitory; projection

383

List the 3 function subdivisions of the cerebellum

1. Cerebro-cerebellum 2. Spino-cerebellum 3. Vestibulocerebellum

384

Cerebro-cerebellum > _____ > UMNs premotor cortex

Dentate nucleus

385

In which cortex of the cerebellum is the cerebro-cerebellum? What is it's associated nucleus? What is it's function?

Posterior lobe; dentate nucleus; influences cerebral cortex in the planning of movements, smoothes out execution of fine motor skills and corrects errors, and determines appropriate muscle tone

386

What are the 2 major inputs and single major output of te cerebro-cerebellum?

Inputs = ponto-cerebellar fibres, inferior olivary nucleus; Output = Thalamus and red nucleus

387

What would be the resultant clinical features of a lesion of the cerebro-cerebellum?

Hypotonia and intention tremor, dysmetria (overshooting targets), dysdiadochokinesia (loss of rhymic control, especially with alternate limb patterns) and loss of timing and speech control

388

Spino-cerebellum > ____ nuclei > UMN motor cortex and brainstem

Interposed

389

What structures make up the spino-cerebellar cortex? What is its associated nucleus? What is its function?

Anterior lobe, vermis and paravermis; globose and emboliform nuclei; adjusts ventral horn activity and coordinates walking

390

List the 2 major inputs and 2 major outputs of the spino-cerebellum

Inputs = spino-cerebellar fibres, inferior olivary nucleus; Outputs = red nucleus and thalamus

391

What clinical features would results from a lesion of the spino-cerebellum?

Ataxic gait, uncoordinated, clumsy movements of the libs (as if drunk) and a stagger to the side of the lesion

392

______-cerebellum > fastigial nucleus > vestibular nuclei

Vestibulo-cerebellum

393

Which parts of the cerebellar cortex make up the vestibulo-cerebellum? What is it's associated nucleus? What is it's function?

Floculonodular lobe, lingula; fastigial nucleus; coordinates posture, eye movements and head position in response to inputs from semicircular canals, visual pathways and extraocular muscles

394

List the 2 major inputs and 3 major outputs of the vestibulo-cerebellum

Inputs = semicircular canals, oculomotor nuclei; Outputs = vestibular nuclei, reticular formation and vestibulo and reticulospinal tracts

395

What clinical features would result from a lesion of the vestibulo-cerebellum?

Ataxic stance (swaying like a todler) and nystagmus (lateral, fast-slow eye movements)

396

Describe the basic information flow through the cerebellum

Input > cerebellar cortex > deep nuclei > output

397

Learning is achieved by synaptic tweaking by ____ fibres from the inferior _____ nucleus

Climbing; olivary

398

List the 4 key circuitry components of the cerebellum

1. Mossy and climbing fibres 2. Granule cells and parallel fibres 3. Purkinje cells 4. Deep cerebellar nuclei

399

Describe the flow of information through the cerebro-cerebellum

Cortex > pons > cerebellar cortex > dental nucleus > red nucleus/thalamus

400

Describe the flow of information through the spino-cerebellum

Spinocerebellar pathways > cerebellar cortex > interposed nucleus (globose + emboliform) > ned nucleus/thalamus

401

Describe the flow of information through the vestibulo-cerebellum

Eye motor cranial nerves and vesticular nuclei > cerbellar cortex > fastigial nucleus > vestibular nucleus/reticular formation