B06W10 Flashcards Preview

Block 6: Neuro > B06W10 > Flashcards

Flashcards in B06W10 Deck (370):
1

Define: nerve

A bundle of nerve fibre along which impulses pass from one part of the body to another

2

Define: root

The origination of a strucutre

3

Define: plexus

An interwoven network of blood vessels, nerves or lymphatics

4

Define: dermatome

The area of skin supplied by a spinal nerve root

5

Define: myatome

the group of muscles supplied by a spinal nerve root

6

List the principal posterior division branches of the brachial plexus

Axillary nerve and radial nerve

7

List the principal anterior division branches of the brachial plexus

Musculocutaneous nerve, medial nerve and ulnar nerve

8

List at least 3 broad causes of pathology to the brachial plexus

1. Structural compression 2. Trauma 3. Iatrogenic 4. Idiopathic 5. Disease of axillary artery/vein

9

List 2 iatrogenic causes of brachial plexus pathology

Radiotherapy, subclavian lines

10

Describe the clinical features when there is damage directly to the brachial plexus

Pain (axilla and down arm), muscle wasting and weakness, sensory loss

11

Describe the surrounding abnormalities seen when there is pathology of the brachial plexus

Axillary/supraclavicular lymphadenopathy, subclavia bruit, cervival rib, lung signs, wounds/arm pathology

12

List the 3 signs of Horner's syndrome that can sometimes be seen accompanying brachial plexus pathology

1. Small pupil 2. Partial ptosis 3. Lack of sweating

13

What may cause Erb's palsy?

Birth injury or other trauma (morotcycle injury) causes lesion of C5, 6 or 7

14

What may cause Klumpke's palsy?

Birth injury causing lesion of C7, 8 or T1

15

List the principal posterior divisions of the lumbar plexus

Femoral nerve and lateral cutaneous nerve of the thigh

16

List the principal anterior divisions of the lumbar plexus

Obturator nerve

17

List the principal posterior divisions of thesacral plexus

Sciatic nerve (c. peroneal) and gluteal nerve

18

List the principal anterior divisions of the sacral plexus

Sciatic nerve (tibial)

19

List at least 5 causes of pathology to the lumbosacral plexus

1. Structural compression (abscess, haematoma, tumour, pregnancy) 2. trauma 3. Iatrogenic (post-surgical, ratiotherapy) 4. Idiopathic lumbosacrel plexopathy 5. Proximal diabetic neuropathy 6. Disease of abdominal aortic aneurism

20

Describe the clinical features of damage to the the lumbosacral plexus

Pain (back, buttock, abdomen, perineum, legs), muscle wasting and weakness, sensory loss and bladder/bowel dysfunction

21

Describe the surrounding abnormalities that may be seen with pathology of the lumbosacral plexus

Abdominal masses, aortic/iliac bruit, mass on rectal examination, wounds, lymphadenopathy, leg pathology

22

Pressure/trauma on nerves can give rise to what sort of nerve pathology? (list all 3)

1. Neurapraxia (myelin damage, conduction slowing and blockage) 2. Axonotmesis (loss of axonal continuity, endoneurium in tact, no conduction) 3. Neurotmesis (entire nevre trunk separated, no conduction)

23

What are the 4 patterns of peripheral nerve lesions?

1. Mononeuropathy 2. Mononeuritis multiplex 3. Multifocal neuropathy 4. Distal symmetrical sensorimotor polyneuropathy

24

List at least 5 differene causes of a peripheral nerve lesion

1. Congenital (hereditary neuropathies) 2. Pressure/trauma 3. Impaired vascular supply (vasa nervorum) 4. Metabolic diseases (diabetes) 5. Infective disorders (AIDS) 6. Nutritional deficiency of B1, B12, folate 7. Toxins 8. Inflammatory

25

List at least 3 routine and 2 special tests for peripheral nerve lesions

Sensory studies, motor stusies and EMG. Special tests = repetitive stimulation and single fibre EMG

26

List the 2 major types of abnormality that can be observed in nerve conduction studies

1. Reduced velocity/increased latency (demyelinating) 2. Reduced amplitude (axonal)

27

Which neve of the lumbar plexus is often pinched in patients who have gained weight?

Lateral cutaneous nerve of the thigh

28

List the 4 parts of upper limb neuro examination

1. Higher cognitive function 2. Cranial nerves 3. Motor examination 4. Sensory examination

29

Which fibres make up the motor pathways in the UMNs

Corticobulbar fibres and corticospinal fibres

30

Which fibres make up the motor pathways in the KMNs

Motor cranial nerves and motor spinal nerves

31

Describe what may be seen in the inspection part of a motor examination of a patient with a lesion

Wasting, fasisculation, involuntary movement, abnormal postures (tone, power, coordination, reflexes and gait changes)

32

What is chorea?

abnormal involuntary movement derived from the Greek word ÒdanceÓ. It is characterized by brief, abrupt, irregular, unpredictable, non-stereotyped movement

33

What is athetosis?

symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue

34

What sort of neurological lesions may cause tremor observed in a neuro exam?

Benign essential tumour, extrapyramidal (parkinsonian) cerebellar

35

Which tremor types are not present at rest and not exacerbated by action, but are exacerbated by posture?

Physiological and benign essential tremors

36

Which tremor type is present at rest, but not exacerbated by exercise or posture?

Parkinsonian tremor

37

Which tremor type is not present at rest or exacerbated by posture, but is exacerbated by action?

Cerebellar tremor

38

What is hemiballism?

very rare movement disorder. It is a type of chorea caused in most cases by a decrease in activity of the subthalamic nucleus of the basal ganglia, resulting in the appearance of flailing, ballistic, undesired movements of the limbs

39

What is catatonia?

Catatonia is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake

40

Wht is gegenhalten?

Paratonia or gegenhalten is defined as "a form of hypertonia with an involuntary variable resistance during passive movement." In other words, attempting to move the limb of a person with paratonia will result in that person involuntarily resisting the movement

41

What is spacticity due to?

Exaggerated stretch reflex in UMN lesions (loss of inhibition to spinal cord)

42

Spacticity due to an UMN lesions is exaggerated by what?

Movement of another limb

43

Rigidity is due to what? What is it associated with and exaggerated by?

Failure of relaxation in extrapyramidal disorders; assoicated with cogwheeling; exaggerated by movement of another limb

44

Describe categories 0-5 of MRC muscle power grading

0 = no movement; 1 = movement of muscle but not joint; 2 = movement if gravity eliminated; 3 = movement against gravity; 4 = movement against resistance; 5 = full power

45

List the muscle, nerve and roots responsible for shoulder abduction

Deltoid; axillary nerve; C5, 6

46

List the muscle, nerve and roots responsible for elbow flexion

Biceps brachii, brachialis and briachioradialis; musculocutaneous nerve and radial nerve; C5, 6

47

List the muscle, nerve and roots responsible for Elbow extension

Triceps brachii; radial nerve; C 6, 7, 8

48

List the muscle, nerve and roots responsible for wrist extension

Ext. carpi ulnaris and ext. carpi radialis; radial nerve; C7, 8

49

List the muscle, nerve and roots responsible for wrist flexion

Flex. Carpi ulnaris and flex. Carpi radialis; ulnar nerve and median nerve; C7, 8

50

List the muscle, nerve and roots responsible for finger extension

Ext. digitorum; radial nerve; C7, 8

51

List the muscle, nerve and roots responsible for finger flexion

Flex. Digitorum superficialis, flex. Digitorum profundus; median nerve and ulnar nerve; C7, 8

52

List the muscle, nerve and roots responsible for finger abduction

Abductor digitorum minimi and first dorsal interosseus; ulnar nerve; T1

53

List the muscle, nerve and roots responsible for thumb abduction

Abductor pollicis brevis; median nerve; T1

54

Give an example of a test of dysmetria (coordination)

Finger-nose test

55

Give an example of a test of rhythm (coordination)

Dysdiadochokinesis

56

Which reflexes are tested in a neuro exam of the upper limb?

Supinator (brachioradialis) jerk, biceps jerk, triceps jerk, finger jerk

57

List the roots that are responsible for the supinator, biceps, triceps and finger jerk reflexes

Supinator (C5, 6), Biceps (C5, 6), Triceps (C7) and finger (C8)

58

List the 4 components of muscle tone that are tested in the neuro examination of the lower limb

1. Assessment of leg tone 2. Spastic catch 3. Ankle clonus 4. Knee clonus

59

List the muscle/s, nerve/s and root/s responsible for hip flexion

Iliopsoas; lumbar plexus and femoral; L1, 2, 3

60

List the muscle/s, nerve/s and root/s responsible for hip extension

Gluteus maximus; inferior gluteal; L4, 5

61

List the muscle/s, nerve/s and root/s responsible for knee extension

Quadriceps femoris; femoral nerve; L3, 4

62

List the muscle/s, nerve/s and root/s responsible for knee flexion

semi membranous, semitendinosus and biceps femoris; sciatic nerve; L5, S1

63

List the muscle/s, nerve/s and root/s responsible for ankle dorsiflexion

Peroneus longus and brevis, tibialis anterior; common peroneal nerve; L4, 5

64

List the muscle/s, nerve/s and root/s responsible for ankle plantar flexion

Gastrocnemius, soleus; posterior tibial nerve; S1, 2

65

List the muscle/s, nerve/s and root/s responsible for ankle inversion

Tibialis anterior, tibialis posterior; cutaneous peroneal nerve and posterior tibial nerve; L4, 5

66

List the muscle/s, nerve/s and root/s responsible for ankle eversion

Peroneus longus and brevis; superficial peroneal nerve; L5

67

List the muscle/s, nerve/s and root/s responsible for big toe dorsiflexion

Extensor hallicus longus; deep peroneal nerve; L5

68

Which tests of coordination should be used in the neuro exam of the lower limb?

Gait, heel-knee shin test, heel shin test

69

Which reflexes should be used in the neuro exam of the lower limb?

Knee jerk, ankle jerk, plantar response

70

Which roots are responsible for the knee jerk reflex?

L3, 4

71

Which roots are responsible for the ankle jerk reflex?

S1, 2

72

What should be observed in neuro examination of gait?

Standing posture, axial tone, righting reflexes (anteropulsion, retropulsion), walking posture and arm swing

73

Compare the types of neurological gait disorders that usually present with unilateral vs bilateral gait characteristics

Unilateral (UMN and LMN), Bilateral (Parkinsonian, marche and petis pas, cerebellar, dorsal column loss

74

List 2 disorders of language processing

1. Aphasia (complete deficit of a particular language skill) 2. Dysphasia (partial deficit of a particular language skill)

75

List and define 3 different types of dysphasia

1. Receptive dysphasia (problem understanding language input) 2. Expressive dysphasia (problem with producing language output) 3. Mixed or global dysphasia (problem with both input and output)

76

What is meant by the 'modular nature of language processing'?

Different elements of language processing and speech production are preformed by different anatomical components of the nervous system

77

List the 3 important anatomical modules responsible for different elements of language processing and speech production

1. Broca's 2. Wenicke's 3. Arcuate fasisculus

78

Which brain structure is considered to be the language input centre?

Wernicke's area

79

Wernicke's area is located directly next to which cortex?

Primary auditory (but only unilateral!)

80

For the majority of both right and left-handed people, which is the dominant hemisphere for language input?

Left (location of Wernicke's area)

81

What important brainstructure is located in the area 22?

Wernicke's area

82

What important brainstructure is located in the areas 44 and 45?

Broca's area

83

What is the language output centre of the brain? Discuss the location of this area

Broca's area: located next to the mouth and tongue parts of the primary motor cortex (only unilateral!)

84

For the majority of both right and left-handed people, which is the dominant hemisphere for language output?

Left (i.e., the same side as Wernicke's area for language input)

85

The major input and output areas for language in the brain are separated by what structure?

Sylvian fissure

86

Describe the shortest available route in the brain for information to be passed from the language input (Wernicke's) to language output (Broca's) areas. What is this direct connection called?

Curves 'arcuate' path runnin around the posterior end of the Sylvian fissure > The arcuate fasiciculus

87

List the 3 main language skills

1. Comprehension 2. Expression 3. Repetition

88

What phrase is used to test repetition as a language skill and why?

No ifs, ands or buts - because it is essentially meaningless

89

If you were to ask a patient to pick up a piece of paper, fold it twice and put it back on the table, what language skill are you testing?

Comprehension

90

How may expression be tested as one of the 3 language skills?

Ask patient to tell you how they would make a cup of tea, or describe to you where they live

91

What is the simplest language task? Which areas of the brain are involved?

Repetition of a spoken phrase: uses all 3 components of language system (Wernickes, arcutate fasisculus and Broca's) but no other language components or connections

92

List the rare dysphasia where the repetition task is the only part of the language system that fails

Conduction aphasia

93

List the rare dysphasia where the repetition task is the only part of the language system that still works

Transcortical aphasia

94

What is 'telegraphic speech'?

Patients use of short grammatical words, with meaning largely conveyed by the main verbs and nouns > test of language expression

95

What is semantic paraphasias?

Patient's use of a word with a neighbouring meaning (arm for leg) > testing language expression

96

What is literal paraphasia?

Use of a similar sounding word (short for stroke) > testing language expression

97

Connections between the language centres of the brain must also involve areas in order to give language meaning. Describe where these connections ppear to be distributed

Diffusely around the border of the language centres - in the neighbouring cortex and in the white matter deep to the language centres

98

Connections between Wericke's area and the rest of the brain enable _____, whilst those between Broaca's and the rest of the brain enable ______

Comprehension; expression

99

The part of Wernicke's area that communicates with the rest of the brain translates _____ into _____, and the part of Broca's that communicated with the rest of the brain translates ____ into ______

Words into ideas; ideas into words

100

Which divisions of language are required for both comprehension and expression?

Vocabulary and grammar

101

What is the lexicon of Wernicke's area?

Mapping between word-sounds and word-meanings (vocabulary)

102

The vocabulary lexicon (mapping between word-sounds and word-meanings) is closely associated with _____ area, whilst the syntactical engine responsible for correct application of grammar rules to sentences is closely associated with _____ area.

Wernicke's area; Broca's area

103

List the 5 types of aphasia, each related to a different site of injury to the language apparatus

1. Wernicke's aphasia 2. Broca's aphasia 3. Conductive aphasia 4. Transcortical sensory aphasia 5. Transcortical motor aphasia

104

Wernicke's aphasia results in loss of which skills?

Comprehension plus word-meanings (vocabulary)

105

Broca's aphasia results in loss of which skills?

Expression plus grammar

106

Conductive aphasia of the arcuate fasisculus results in loss of which skills?

Repetition

107

Transcortical sensory aphasia results in loss of which skills?

Comprehension (but preserved repetition)

108

Transcortical motor aphasia results in loss of which skills?

Expression (but preserved repetition)

109

Transcortical sensory and transcortical motor aphasias both result in preservation of which language skill?

Repetition

110

Describe the hallmarks of Broca's aphasia

Complete failure at the expression phase of language processing, which affects both expression of the patient's own ideas as well as repetition

111

Describe the pattern of speech seen in Broca's aphasia

Slow, hesitant, non-fluent and syntactically simple > telegraphic

112

Broca's aphasia is also known by what other name?

Expressive dysphasia

113

Describe the patient experience of Broca's aphasia

Patient usually frustrated

114

List the 2 main reasons why comprehension may be mildly impared in Broca's aphasia

1. May be mild damage to Wernicke's area 2. The syntactical engine is likely to be damaged in Broca's area, so sentences requiring complex phrasing may be misinterpreted

115

What is the hallmark of Wernicke's aphasia?

Impaired comprehension - questions not answered appropriately and complex commands not carried out. Repetition can be impossible in a complete case (and because of interdependence of Wernickes and Brocas, the are major impairements in expression also)

116

Wernicke's aphasia is also known by which other name?

Receptive aphasia

117

Why are paraphasias common in Wernicke's aphasia?

Because there is lexical impairement and poor mapping of sounds to meanings, causing word substitutions

118

Describe the patient experience of Wernicke's aphasia

Often anosognosia (unawareness of the deficit) - patients cannot self-monitor speech or comprehend the first part of the sentence whilst trying to express the second half

119

What sort of aphasia produces fluence and grammatically normal speech, but with empty and meaningless content littered with phonemic and sematic paraphasias?

Wernicke's aphasia

120

Discuss what is seen in complete global aphasia

Both comprehension and speech absent - patient reduced to single words and may only understand simple questions or single-word prompts

121

Discuss what is seen in an incomplete case of global aphasia/mixed dysphasia

Incomplete impairement in comprehension and expression. Speech is non-fluent and littered with errors. Patient often has enough self-monitoring to release they have used the wrong word and may make several attempts to correct it. Usually expressive problems are most obvious to the patient and examiner

122

Describe the location of a lesion producing transcortical aphasia?

Lesion not intrinsic to language areas but to their connections with the cortex

123

What is the hallmark of transcortical aphasia?

Intact repetition (in conjunction with a comprehension problem as in sensory transcortical aphasia, an expression problem as in motor transcortical aphasia, or both as in mixed transcortical aphasia)

124

Name the type of aphasia causing a patient to perceive their own language as foreign, whether spoken by others or attempted by themselves. Phrases can be repeated but with an impaired understanding of what they mean.

Mixed transcortical aphasia

125

What is the hallmark of conduction aphasia?

Impaired repetition, in the presence of normal comprehension. Ideas are understood and then re-expressed, but the original words are lost, as though repeating a story a day later

126

What is anomia?

The inability to nme objects

127

Many dysphasia recover to leave a mild ____ as the only residual sign

Dysnomia (difficulty naming objects)

128

In any language disorder, what other condition should be considered? What should be tested in these cases?

Delirium: non-verbal behaviour should be assessed to determine whether the problem extends beyond language

129

Broca's area is supplied by which vessel?

Superior division of the middle cerebral artery

130

Wernicke's area is supplied by which vessel?

Inferior division of the middle cerebral artery

131

In most stroke patients with dysphasia, the infarct is in the territory of which artery?

Left middle cerebral artery

132

Explain why patients with a middle cerebral artery stroke often have either a nearly global aphasia or a mised dysphasia

Global aphase because of involvement of both divisions of the artery (superior supplying Broca's and inferior supplying Wernicke's); Mixed dysphasia because the vascular supply is not neat and cleacut, so can impinge on other areas

133

What is the main cause of transcortical aphasia?

Watershed infarction of the structures at the edge of the middle cerebral artery territory

134

If there is a watershed infarction between the middle cerebral artery and anterior cerebral artery, which aphasia is produced and why?

Motor transcortical aphasia, because Broca's area is isolated

135

If there is a watershed infarction between the middle cerebral artery and posterior cerebral artery, which aphasia is produced and why?

Sensory transcortical aphasia, because Wernicke's area is isolated

136

What is a watershed infarct or watershed stroke?

Ischemiae localised to the border or zone between the territories of two major arteries

137

Discuss the non-language related findings seen in Broca's aphasia due to the arrangement of the motor humunculus

Weakness of the right face and right arm and dysarthria

138

Discuss the non-language related findings seen in Wernicke's aphasia

Weakness and dysarthria usually mild or absent and a contralateral visual field defect is common, especially affecting the right upper quadrant

139

What skill can be used to provie that dysphasia is not present and that a problem with auditory comprehension or speech has another cause?

Completely normal reading and writing skills

140

What must be excluded before making a diagnosis of alexia or agraphia?

Simple sensory and motor deficits

141

What is Gerstman's syndrome?

Lesion of the dominant parietal lobe causing right-left agnosia, agraphia, acalculia and finger agnosia (RAAF)

142

What is dysarthria?

Motor impairement of the mouth, tongue or pharynx, leading to slurred or poorly articulated speech (no problem with language processing or word selection)

143

List at least 4 potential causes for dusarthria

Diffuse CNS impairement (drunk), cerebellar lesion (stroke), UMN lesion, LMN lesion (CN VII and XII), lesion of NMJ (myasthenia gravis), non-neuromuscular mechanical lesion (cleft palate, loose dentures etc.)

144

LMN lesions of which 2 cranial nerves most commonly cause dysarthria?

CN VII (facial) and CN XII (hypoglossal)

145

Describe the differences between spastic and non-spastic dysarthria

Spastic: slow, sustained with longer time spend on some syllables than is usual, and looks effortful; non-spastic: speech proceeds with normal rhythm but consonants are pronounces indistinctly, so it resembles severe mumbling

146

What is the hallmark of any cerebellar motor impairement?

Motor components put together awkardly with impaired temporal patterning, difficulty with rapid sequences (dysdiadochokinesis) and failure to scale the effort of the movements accurately (dysmetria)

147

Describe the characteristics of cerebellar (scanning) dysarthria

Irregular rhythm with some syllables slower and some faster than usual, and some too loud or soft with unexpected breaks within words or words joined together

148

Cerebellar dysarthria may be difficult to distinguish between which other speech condition?

Spastic dyarthria

149

If a patient has no speech at all (anarthria), how can you tell the difference between anarthria and aphasia?

Look for other motor problems involving the mouth and pharynx, look for other language deficits (as in reading and writing) and consider the deficits in the recovery phase

150

What is dysphonia? What are the characteristics of pure dysphonia?

Impairement of voice production; language normal and whispering speech noral, but voices speech is too quiet or hoarse

151

List some of the possible causes of dysphonia

Lesions of laryngeal nerve, larynx, respiratory weakness

152

In dysphonia, weakness of one vocal cord usually causes _____, whilst weakness of oth causes _______ and, if severe, may cause ______ due to inspiratory obstruction

Hoarseness; whispering; stridor

153

List at least 4 common pathologies of the auditory system

1. Deafness (presbyacusis) 2. Tinnitus 3. Meniere's disease (bouts of fluculating deafness, dizziness, low-frequency tinnitus and sometimes a feeling of fullness in the ear) 4. Hearing-balance interactions

154

What are the 2 distint streams of hearing loss?

1. Conductive hearing loss 2. Sensorineural hearing loss

155

What is conductive hearing loss caused by?

Loss in transmission of sound from the outer ear to the inner ear

156

What is sensorineural hearing loss due to?

Damage somewhere in the pathway from the hair cells to the cortex

157

In hearing loss, which frequencies are the first to be lost?

Higher

158

In an audiogram, 0 dB corresponds what pressure?

20 micro pascals

159

What range of volume corresponds to normal hearing?

0-20 dB = normal hearing

160

Why is conversation in a noisy room particulary difficult for people with hearing loss?

With hearing loss, need louder sound to hear higher frequencies > tend to lose ability to hear consonants

161

List at least 4 causes of conductive hearing loss

1. Blockage of the outer ear by wax 2. Fluid in the middle ear (glue ear) caused by infections of the middle ear (otitis media) 3. Otosclerosis in which the ossicles of the middle ear harden and stiffen 4. Damage to the ossicles from infection or head injury 5. Perforated eardrum from infection or injusry

162

Ear wax is also called ____, and is secreted by the ____ glands in the ear canal

Cerumen; cerumenous

163

What is the purpose of ear wax?

Renders the ear 'self-cleaning'

164

What are the 2 types of ear wax?

Wet (most genes) and dry (north Asian genes)

165

What is the most common cause of hearing loss? Comment on some of the sequelae of this.

Blockage of the ear canal with wax > can lead to earache, fullness, tinnitus, itch.

166

What is the remedy for a blocked ear canal due to wax?

Ear drops to soften and then syringe with warm water (use of an electric pump most effective)

167

List at least one common ear infection affecting the outer ear, middle ear and cochlea. List also the remedy for these conditions.

Outer = swimmer's ear (mild antibiotic drops); Middle = infection glue ear where there is blockage of the Eustacian tube, preventing the equalisation of pressures across the ear drum (not bacterial so antibiotics unhelpful, can use Grommets in tympanic membrane to ventilate the ear); Cochlea = viral inflammation occasionally

168

In which condition are grommets helpful?

Middle ear infection (glue ear) where there is blockage of the eustacian tube (inserted into tympanic membrane to ventilate the ear)

169

List at least 5 causes of sensorineural hearing loss

1. Age-related hearing loss (presbyacusis) due to loss of hair cells 2. Acoustic trauma from loud noise damaging hair cells 3. Infections causing loss of hair cells and damage to auditory nerve 4. Meniere's disease 5. Powerful antibiotics 6. Acoustic neuroma (benign tumour affecting the auditory nerve) 7. Congenital abnormalities causing dysfunctional hair cells 8. Other neurological conditions such as MS, stroke or brain tumour

170

Loud noise leads to damaged _____, then loss of _____ _____, and then loss of auditory ______

Steriocilia; hair cells; neurones

171

What is the principal sensory diability in Australia?

Adult-onset hearing loss

172

What are the 2 most common forms of hearing loss?

Noise-induced hearing loss (NIHL) and ageing (presbycusis)

173

There is a correlation between hearing loss and tinitus ______

Frequency

174

Many people with tinnitus can modulate the frequency or loudness by what means?

Oral or facial movement or pressure (CN VII and VIII)

175

Which 2 substances can induce tinnitus?

Salicylate (aspirin) and quinine

176

What is tinnitus usually associated with hair cell loss from what situations?

Ageing, noise or some diseases

177

Why is it thought that CNs VII and VIII are assocaited with tinnitus?

Because tinnitis can be modulated by different oral movement and facial expression

178

What are the current approaches for treating tinnitus?

No direct therapy: approches involve noise makers and cognitive retraining therapy. Hearing aids are also shown to improve distress scores by masking tinnitus sound by turning up other background sound. Cochlear implants abolish tinnitus in 20% of cases and reduce it in 50%

179

What is Meniere's disease characterised by?

Sudden attacks of dizziness, fluctuating, hearing loss, low frequency tinnitus

180

Describe the theory of Meniere's disease as caused by overactivity of the middle ear muscles

Activation of middle ear muscles can push on the stapes and cause the hydraulic pressure inside the labyrinth to increase. Overpressure in the labyrinth is known to cause dizziness, hearing loss and tinnitus (and sometimes feeling of aural fullness)

181

In terms of evolution, the cochlear is an appendix to which other structure of the inner ear?

Saccule

182

Endolymph is created in which structure?

The endolymphatic sac

183

Compare and contrast the different symptoms that are produced from sounds vs position

Sounds can induce dizziness whilst position can induce vertigo and tinnitus

184

What is otosclerosis?

A hereditary disorder causing progressive deafness due to overgrowth of bone in the inner ear (can cause stapes to become wedged in the oval window)

185

What are the advantages and disadvantages of digital vs analog hearing aids for deafness?

Analogue cheaper but limited adjustments; digital can be tuned ot the ear but they are more expensive and there is a problem of time delay

186

How does a cochlear implant work?

Wire of electrodes inserted into the cochlear - each electrode is tuned to a different frequencies, as the normal hairs are

187

What are the 3 more common forms of cochlear implants?

1. Nucleus 2. Advanced bionics 3. Med-El

188

What is presbyacusis?

Presbycusis is the most common type of Sensorineural Hearing Loss caused by the natural aging of the auditory system. It occurs gradually and initially affects high frequency sounds (10kHz) and progressively moves down to lower frequencies (1kHz and below)

189

Why are cochlear implants thought to be more helpful for children and less useful for the elderly?

Because there is a component of learning involved (nothing sounds the same anymore, including your own voice)

190

What types of CNS infections are uniformly fatal or have a high risk of significant morbidity if treatment is delayed?

All CNS infections with the exception of viral meningitis

191

What forms the blood brain barrier?

Endothelium lining the brain capillaries

192

List the 4 main structural components and associated functions of the BBB

1. Intercellular tight junctions (limit paracellular flux) 2. Lmited pinocytotic activity (limit transcellular flux) 3. Additional physical protection with basement membrane and astrocyte foot processes 4. Specific carrier and transport systems

193

What is the main purpose of the BBB?

Forms a continuous barrier between the blood and brain that restricts the transport of ions, molecules, cells and pathogens

194

Which 2 layers make up the dura mater?

1. Periosteal layer 2. Meningeal layer

195

The superior sagittal sinus is filled with _____ blood

Venous

196

Which dural space contains the CSF?

Subarachnoid

197

At which location is CSF produced?

Choroid plexus

198

How much CSF is produced and recirculated each day?

400-600ml

199

Compare the normal CSF volume in newborns vs adults

Newborns = 10-60ml; Adults = 100-160ml

200

CSF represents a rich and sterile ____ media

Microbial

201

What analysis is important in the diagnosis of CNS infections?

Analysis of CSF

202

The choroid plxus consists of an abundance of ____ separated from the _____ by choroid ____ cells

Capillaries; ventricles; choroid epithelial cells

203

Choroidal epihtelial cells are continueous with which other cells that line the ventricles?

Ependymal

204

What is the purpose of tight junctions between choroidal epithelial cells?

Prevent majority of substances from crossing the cell layer into the CSF

205

What component of the CSF makes it a rich environment for microbial growth?

High glucose content

206

The subdura is between the __ mater and the ____ mster

Dura mater; arachnoid mater

207

Where is the epidural space?

Outside the dura mater in the spinal canal

208

List common mechanisms/pathway and 2 less common mechnisms of CNS infections

Common = Physical pathway, haematogenous pathway; Uncommon = peripheral nerve pathway, olfactory nerve pathway

209

List at least 3 ways in which the BBB/BCB may be physically compromised

Congenital defect, trauma or surgery, extensions from bone infections resulting from dental, chronic sinus, mastoid, or middle ear infections and vertebrodiscitis

210

What is the difference between a primary blood infection and secondary blood infection?

Primary = blood infection after entry to body (usually via respiratory tract); Secondary = blood infection from primary focus of infection elswewhere (as in penumonia and meningitis or endocarditis with stap brain abscess)

211

Give an example of a CNS infection that spreads via the peripheral nerve pathway

HSV 1 encephalitis, rabies encephalitis (lyssavirus)

212

Using rabies as an example, explain the pathogenesis of CNS infection as spread via the peripheral nerve pathway

1. Virus enters hose via animal bite 2. Virus resplicated in msucle at the site of bite 3. Virus infects nerve in peripheral nervous system and moves by retrograde transport 4. Virus replicated in dorsal root ganglion and travels up spinal cord to brain 5. Brain becomes infected 6. Virus travels from brain via nerves to other tissues such as eye, kidney, salivary glands etc. (uses ascending tracts to get to the brain adn then the descending tracts to get back down and cause motor effects etc.)

213

Which animal spreads the rabies virus in Australia?

Australian Bat Lyssavirus (ABL)

214

Describe the mechanism of HSV1 encephalitis

Primary infection can travel along the nerve and become latent in the dorsal root ganglion. The virus can reactivate at any time, and travel back along nerve to cause lesions on the face, or may also progress forward and onto/into the CNS

215

Where does amoebic meningoencephalitis most often stem from?

Warm bodies of fresh water (esp tropical)

216

Which pathogen is the main cause of amoebic meningoencephalitis?

Naegleria fowleri

217

Confusion, seizures and/or neurological deficits suggests what types of CNS infections?

Encephalitis, myelitis or focal lesions/abscesses

218

List a few manifestations of CNS infections other than in the CNS

Rash, pneumonia, sinusitis, otitis media

219

List the 4 infectious causes of meningitis, and comment on their severity

1. Bacterial - fatal without antibiotics 2. Viral - most common, usually self limiting 3.Fungal - uncommon and fatal without antifungals 4. Parasitic - uncommon but high mortality

220

List 3 non-infectious causes of meningitis

Autoimmune diseases, drugs and malignancy

221

What are the risk factors associated with bacterial meningitis from strep pneumoniae?

Hyposplenism, extremes of age, HIV infection, hypogammaglobunaemia (MM)

222

Mastoiditis, sinusitis, otitis media, pneumonia and bacteraemia are associated with bacterial meningitis from which organism?

Strep pneumoniae (gram positive diplococci)

223

Bacteraemia with a rash is associated with bacterial meningitis from which organism?

Neisseria meningiditis (gram negative diplococci)

224

Subacute zoonosis from unpasteurised dairy products, deli meat and salads are associated with bacterial meningitis from which organism?

Listeria monocytogenes (gram positive bacilli)

225

Maternal colonisation and chorioamniotitis are associated with bacterial meningitis from which organism?

Group B strep (gram positive cocci in chains)

226

Subacute-chronic presentation wand tuberculomas are associated with bacterial meningitis from which organism?

Mycobacterium tuberculosis (acid fast bacillus)

227

What are the risk factors associated with bacterial meningitis from neisseria meningiditis?

Less than 2 years and 15-25 years old, complement deficiency

228

What are the risk factors associated with bacterial meningitis from listeria monocytogenes?

Immunosuppressed (T cell deficiency), pregnancy and neonates

229

What are the risk factors associated with bacterial meningitis from group B streptococcus?

Neonates - early onset within first week of lide, late onset 1-4 weeks of life

230

What are the risk factors associated with bacterial meningitis from mycobacterium tuberculosis?

TB exposre in the past, reactivation, immunosuppression

231

Which viruses can cause meningitis? (Name at least 3)

Enterovirus (picornavirus), herpes simplex (human herpes virus), varicella-zoster (human herpes virus) and primary HIV (retrovirus)

232

Which 2 fungi can cause meningitis (uncommon). Comment on which populations/exposure groups these effect

1. Cryptococcus neoformans (mainly immunosuppressed, T cell deficienct HIV cases) 2. Cryptococcus gatii (red river gums)

233

Describe the onset of meningitis from a fungal agent

Subacute - chronic

234

What may be a complication of meningitis caused by a fungal agent, which is also often seen in TB cases?

Meningeal inflammation may result in cranial nerve palsies (similar to TB)

235

What is acute viral encephalitis/myelitis caused by?

Direct viral infection of neuronal cells

236

What is post-infectious encephalomyelitis/myelitis caused by and what is a key feature? When does this usually occur?

Immne-mediated; peri-venular inflammation and demyelination (e.g., post-measles)

237

What are the most common viral causes of encephalitis and myelitis?

Herpes simplex 1/2, enterovirus including polio, varicella zoster, CMV, arboviruses (Australian encephalitis, Japanese encephalitis, West Nile virus), rabies and hendra

238

What are the most common bacterial causes of encephalitis and myelitis?

Listeria monocytogenes, mycoplasma pneumoniae

239

What are the most common parasitic causes of encephalitis and myelitis?

Naegleria fowleri, acanthomoeba, trypanosoma brucei, cysticercosis

240

List the types of infections and types of pathogens that are commonly responsible for continguous focus brain abscesses

Otitis media, sinusitis, dental infection; usually polymicrobial including strep anaerobes and gram negatives

241

List the types of infections and types of pathogens that are commonly responsible for brain abscesses via haematogenous spread

Lung abscess (strep milleri, anaerobes, mycobacterium tuberculosis), infective endocarditis (staph aureus)

242

What is the most common pathogen that can cause brain abscess via trauma or post-surgical infectious spread? Where would this spread from to cause infection?

Staph aureus (from skin or upper respiratory tract flora from sinuses)

243

List 3 unusual microorganisms that can cause infectious brain abscess in immunocompromised hosts

1. Toxoplasmosis (HIV) 2. Nocardia 3. Fungal infections (neutropenic)

244

How can infectious brain abscesses be differentiated from other mass lesions (such as neoplasms)?

Clinicaly behave same as other mass lesions, but may also have associated fever

245

What is a spinal epidural abscess?

Collection of pus (can cause irreversible damage) between outermost layer of meninges and the vertebral column

246

What are the serious sequelae of spinal epidural abscesses that cause them to be classified as medical emergencies?

May cause irreversible paraplegia or quadriplegia due to cord compression or infarction

247

List at least 4 ways that a spinal epidural abscess may form

Haematogenous spread, direct extension from osteomyelitis/discitis, penetrating injury, extension from a decubitus (pressure) ulcer, post procedure (surgery, LP, epidural anaesthesia)

248

Describe the presentation of spinal epidural abscess

Fever, very severe local vertebral pain, radicular pain, neurological impairement

249

What are the 2 most common pathogens causing spinal epidural abscess

1. Staph aureus (up to 90%) 2. Mycobacterium tuberculosis (endemic regions - i.e., this will be more or less likley depending on the exposures of the patient)

250

What CNS infections can be diagnosed with the use of CT/MRI?

Encephalitis, brain anscess, epidural abscess

251

What CNS infection can be diagnosed with the use of EEG?

Encephalitis

252

List at least 4 microbial investigations used in the diagnosis of CNS infections

1. LP - CSF analysis 2. Abscess aspirate - culture 3. Tissue biopsy - histology and culture 4. Blood cultures 5. Immunoassay - antibody/antigen detection

253

What are the 4 routine tests performed on a lumbar puncture investigation?

1. Opening pressure 2. MCS (cell count and gram stain) 3. Protein 4. Glucose

254

What volume of CSF should be collected in a lumbar puncture?

3-4 tubes of about 2mL each = total volume of collection = 8-10mL (this is quite a lot and explains why patients may develop a headache after the procedure)

255

Meningitis from what pathogen results is the highest CSF WCC? Which is lowest?

Bacterial and fungal high, bacterial lower

256

What is the typical picture of a WCC differential in CSF?

All mononuclear

257

Meningitis from which pathogens result in a mononuclear predominance in the WCC differential of a lumbar puncture sample?

Viral and fungal

258

Meningitis from which pathogen results in a polymorphic predominance in the WCC differential of a lumbar puncture sample?

Bacterial

259

What is the normal range of protein in the CSF?

150-450mg/L

260

Meningitis from which pathogens tends to show a more marked increase of CSF protein?

Bacterial and fungal

261

What is the normal range of glucose in the CSF?

more than 2/3 serum

262

Meningitis from which pathogens causes a marked decrease in CSF glucose (to less than 2/3 serum?)

Bacterial and fungal

263

What would typically be detected in the CSF glucose levels of a patient with a viral meningitis?

Normal or slightly low levels (i.e., not as marked as bacterial or fungal causes)

264

What is the normal opening pressure of a lumbar puncture?

8-21 cm of water

265

Which pathogen consistently causes raised opening pressure of a lumbar puncture in meningitis?

Bacterial (as opposed to viral and fungal which are more variable)

266

List 4 additional (non-routine) tests that can be done on a lumbar puncture, and comment on what each is useful for

1. Special stains (i.e., Giemsa for eosinophils and amoeba - parasites) 2. Antigen tests (strep penumoniae) 3. Special culture (mycobacterial) 4. Molecular tests (HSV, enterovirus, meningo/pneumococcus)

267

A 22 year old (otherwise fit and healthy) woman presents with 3 days of URTI symptoms. She now has acute onset of fever, headache, photophobia and increasing confusion. What do you suspect? What tests do you order?

Neisseria meningiditis (CSF for infection and pathogen type and gram stain and PCR to identify pathogen)

268

A 52 year old man presents with 2 days of mild-moderate fevers and unusual behaviour, including confusion, dressing inside out, wearing reading glasses whilst driving. He has had 12 months of frontal headaches, drinks heavily and has poor dentition. What do you suspect? What should you order?

Infective brain abscess or cancer; order brain MRI/CT, biopsy of lesion with mcs

269

A 56 year old man presents with 2 day history of fever, headache and lethargy, unusual behaviour and expressive dysphagia. What do you suspect? What tests should you order?

HSV1 - Herpes simplex encephalitis (CSF - protein will be high, PCR shows HSV1)

270

Which lobes of the brain are commonly affected by herpes simplex encephalitis, and what behavioural changes does this correlate with?

Temporal and frontal lobes = dysphagia and behavioural changes, as well as possible seizures

271

List 3 tests used to diagnose herpes simplex encephalitis

CSF PCR for HSV1; EEG showing temporal spike and wave pattern; MRI will be abnormal in a large percentage

272

What is used in the immediate treatment of herpex simplex encephaltiis (medical emergency)?

Acyclovir as soon as possible

273

Why are antibody tests for HSV1 encephalitis NOT useful diagnostically in an acute setting?

May occur with primary or reactivation of HSV infection > with or without cutaneous lesions. Most people have already had it, so will test positive anyway.

274

What does HSV IgG seroconversion indicate?

Recent HSV1 infection

275

When should a strep pneumoniae test be requested on CSF testing?

When suspecting CNS infection in a patient who has had a splenectomy

276

Stimulating the brain near the junction of the pons and midbrain produces?

Arousal (reticular activating system)

277

Stimulalting the thalamus at low frequency induces what state?

Sleep

278

The reticular formation interconnects which 3 major functional structures?

Brainstem, limbic system and neocortex

279

The reticular formation runs from the caudal ______ to the rostral _____

Medulla; midbrain

280

Which diffusely organised area forms the central core of the brainstem?

Reticular formation

281

What is meant by the 'convergence and divergence' of the reticular formation?

Single cells are able to respond to different modalities/stimuli

282

Which NTs are active in the reticular activating system?

NA, 5-HT, orexin, dopamine, ACh

283

Name at least 4 structures which are influenced by the reticular activating system

1. Thalamus 2. Cortex 3. Ventral stream: hypothalamus/ANS, basal forebrain 4. Dorsal stream: projected via thalamus to the cortex and some spinal cord 5. Motor control (due to projection down into the spinal cord)

284

Describe the location of serotonin NT in the reticular activating system

Centrally

285

What sort of physiological functions are achieved by sleep?

Energy conservation, consolidation of memory, replenishment of brain glycogen levels (which drop on waking)

286

Which brain structure predominantly controls circadian rhythms?

Hypothalamus

287

How much sleep does an average human need?

7-8 hours at a circadian rhythm between 10:30pm-6:30am

288

Describe the way that sleep requirements differ throughout the lifespan

Sleep requirement decreases with age

289

Neurodegenerative disorders all result in what other type of disorder?

Sleep

290

Why do juveniles have a circadian rhythm shifted to a later window?

Due to sex hormones (need more sleep ins and longer hours, etc.)

291

Can sleep deficits be accommodated by proceding sleep?

Yes, short deficits can be commondated with few subsequent longer sleeps

292

How many stages of sleep are there?

Stage 1-4 + REM

293

Stage I sleep is dominated by what sort of frequencies?

Theta frequency 4-8Hz and amplitude)

294

Stage II sleep is dominated by what sort of frequencies?

Alpha waves 10-12 Hz with spindles (50-150 micro V)

295

Stage 3 and 4 sleep are collective known as what sort of sleep?

Deep sleep

296

Descent into deep sleep takes how long?

1 hour

297

Describe the changes in the ANS that occur during REM sleep

Increased HR, resp rate and erection

298

In what steep state does dreaming occur?

REM

299

What is dreaming?

Unique state of awareness that entails features of memory and hallucinations > without sensory stimuli

300

Describe the movement of the body during REM

Rapid eye movements but all other muscles quiet (except penile erections)

301

Sleep walking and talking occur during which sleep type?

Non-REM

302

List 2 areas of the cortex that are inactivated during REM sleep and 3 areas that are activated during REM

Inactivated = dorsolateral prefrontal cortex and posterior cingulate gyrus; Activated = anterior cingulate gyrus, amygdala and parahippocampal gyrus (i.e., limbic system)

303

Which NT system is activated during REM sleep?

Cholinergic neuromodulatory system (but all others are downregulated, so neural activity increased)

304

Discuss the nuclei regulating the sleep/wake cycle

Central is histamine from tuberomammillary body in hypothalamus. Hypothalamus-RAS interaction: Ventrolateral preoptic nucleus promotes sleep, and ablation of this causes insomnia. Orexin-ergic system promotes eakefulness

305

Name the 2 states that the thalamus can be in

1. Regular firing mode 2. Bursting firing mode

306

Discuss the firing of neurons in the thalamus in sleep vs wake

Highly synchronised burting in thalamic cells during sleep, but maintained firing when awake

307

Describe the physiology of sleep spindles on EEG

Thalamic reticular cells inhibit thalamocortical cells causing hyperpolarisation which activates T-type calcium channels to generate spike-lets and calcium spike (burst), which then positively feeds back onto reticular cells > functional disconnectedof cortec from inputs (i.e., sleep spindles reflec bursts of thalamic activity in the cortex)

308

Why is there a diminshed response to sensory stimuli in sleep?

Dorsal RAS inhibtis dorsal columns via GABA

309

What causes muscle relaxation in sleep?

Glycine release from interneurons activated via reticulospinal projections

310

Which muscles do NOT relax in sleep?

Muscles that keep the pharynx/larynx open and respiratory muscles

311

List 4 sleep promoting areas

1. Dorsal reticular formation 2. Solitary nucleus 3. Ventrolateral preoptic nucleus 4. Basal forebrain

312

List at least 5 sleep activating systems

Medial reticular formation, orexin, locus ceoruleus, raphe nucleus, tuberomamillary nucleus and forebrain

313

How do benzodiazapines/barbituates affect sleep?

Fast sleep onset into S1 very fast, causes prolonged deep sleep, but decreased REM sleep > people still feel tired when they wake up, even though they achieved sleep quickly > also create lasting hangover as some have long half life

314

How does caffeine (or stimulants) affect sleep?

Delays descent into deep sleep with re-awakening and shortens overall sleep, REM and deep sleep

315

Arousal is a behavioural manifestation of ____ activation

CNS

316

Describe the mechanism of arousal

Arises as a consequence of activation of all neuromodulatory systems. Switched on my ypothalamic interactions (His) via negative feedback onto VLPM. If switched on, person can become conscious

317

In REM sleep, the ___ system is active, whilst the ____ cortex is not

Limbic; prefrontal

318

Which nucleus is the 'driver' of sleep, how does it work?

Ventrolateral preoptic nucleus in hypothalamus - shuts the histaminergic activation down

319

Activation of the RAS system and all neuromodulatory systems has what effect?

Arousal (increased alertness, orientation, attention, action or emotion)

320

List the 4 components of the basal ganglia

1. Striatum 2. Pallidum 3. Subthalamic nucleus 4. Substantia nigra

321

What are the 2 regulators of the basal ganglia?

Subthalamic nucleus and the substantia nigra

322

Name the 2 structures of the striatum

Caudate, putamen (nucleus accumbens)

323

Name the 2 structures of the pallidum

Globus pallicus - medial/internal and lateral/external segments (includes substantial nigra 'pars reticulata'

324

List the 4 pathways that are under control of the motor cortex

Red nucleus (rubrospinal), corticospinal, reticulospinal (through reticular nuclei) and tecto-spinal (through superior colliculus and vesticular nuclei)

325

List the 2 lateral pathways controlled by the motor cortex

Rubro spinal and corticospinal

326

List the 2 ventromedial pathways contolled by the motor cortex

Reticulospinal and tectospinal

327

Describe the locations of the corticospinal tracts in a spinal cord segment

Lateral tract runs laterally to dorsal horn (large area) and ventral tract runs just laterally to the anterior median fissure on the anterior part of the cord

328

Describe the locations of the rubro spinal tract in a spinal cord segment

Just anterior to lateral corticospinal tract (lateral to dorsal horn)

329

Describe the locations of the reticulo spinal tracts in a spinal cord segment

Lateral (medullary) tract is lateral to anterior horn, medial (pontine) tract is medial to anterior horn, closer to midline (i.e., these two tracts kind of sandwhich the anterior horn from either side)

330

Describe the locations of the tecto spinal tract in a spinal cord segment

Most anterior descending tract, lying just lateral to the anterior median fissue and just below the ventral cortico spinal tract

331

What are the lateral and medial reticulospinal tracts responsible for?

Locomotion and postural control

332

What are the lateral and ventral corticospinal tracts responsible for?

Conscious control of movement

333

What is the tectospinal tract responsible for?

Head positioning reflexes

334

What is the caudate connected to, and what does it influence?

Connected to frontal and pre-frontal areas and posterior parietal cortex; influences social and moral behaviours

335

When is the caudate most active?

During the acquisition of new motor skills - planning ahead during more complex motor intentions

336

Where is the putamen mainly connected to?

Somatic cortical areas (somatosensory cortex and primary motor cortex in pre and post central gyrus) and has a mapped representation of the body

337

What inputs supply the caudate?

Cortex, SNpc, prefrontal cortex, parietal cortex

338

What inputs supply the putamen?

Cortex, SNpc, SMA (supplementary motor area), M1 (primary motor cortex) and S1 (somatosensory cortex)

339

What is the output of the neostriatum? What type of NT do they carry?

Globus pallidus; largely GABAergic (inhibitory)

340

List 4 loops of the basal ganglia that each influence different motor behaviours, and state the main nuclei of each loop

1. Motor loop (putamen) 2. Cognitive lop (caudate) 3. Limbic loop (nucleus accumbens) 4. Occulomotor loop (caudate)

341

What is the motor loop of the basal ganglia responsible for?

Scaling strength of muscle contractions in collaboration with supplementary motor area (putamen provides a reservoir of learned programs)

342

Which basal ganglia nucleiprovides a reservoir of learned motor programs?

Putamen

343

What is the cognitive loop of the basal ganglia responsible for?

Planning ahead for motor intentions (once learned, progresses to motor loop)

344

What is the limbic loop loop of the basal ganglia responsible for?

Reward and emotivational behaviours, memory and any motor expression relevant to emotions (smiling/guesturing etc.)

345

Problems with the occulomotor loop of the basal ganglia causes which signs/symptoms of parkinsons disease?

Saccades (rapid movement of the eye between fixation points)

346

Damage to which basal ganglia loop is responsible for problems with expression in parkinsons disase?

Limbic loop (via nucleus accumbens)

347

Describe the basic pathway of a typical basal ganglia motor circuit

Intention/plan of movement from frontal, parietal, temporal lobes etc. sent to basal ganglia, which integrafes inputs to determine correct program. Sends signals via thalamic nuclei through supplementary motor area to primary motor cortex, and this producted the action

348

State the pathway of the limbic basal ganglia loop

Limbic cortex > nucleus accumbens > MD of thalamus > inferior pre-prontal cortex

349

State the pathway of the cognitive basal ganglia loop

Prefrontal/premotor cortices > putamen, caudate and globus pallidux > VA of thalamus > supplementary motor area

350

Where is the nucleus accumbens located within the basal ganglia?

Anterior end of putamen/caudate and connected to inferior prefrontal cortex (limbic system)

351

The limbic basal ganglia loop is rich in which NT?

Dopamine

352

State the pathway of the oculomotor basal ganglia loop

Frontal eye fields/PCC > caudate and SNr (under regulation from superior colliculus) > Va of thalamus > frontal eye fields

353

Describe what happens in the oculomotor loop of the basal ganglia in eye fixation vs saccade

SNpr tonically inhibits cells in the superior colliculus. When a deliberate saccade is about to be made, SNr activity stops to disinhibit superior colliculus

354

List the cortical targets of the motor loop of the basal ganglia

Primary motor, premotor and supplementary motor cortices

355

List the cortical targets of the oculomotor loop of the basal ganglia

Frontal eye fields, supplemerary eye fields

356

List the cortical targets of the prefrontal loop of the basal ganglia

Dorsolateral prefrontal cortex

357

List the cortical targets of the limbic loop of the basal ganglia

Anterior cingulate, orbital frontal cortex

358

List the basal ganglia structures involved in the regulation of motor acitvity

6 pairs of nuclei: caudate, putamen, globus pallidus, subthalamic nuclei, SN, pedunculo-pontine nuclei (brainstem)

359

Name the 2 pathways from the cortex responsible for the initiation and execution of voluntary movement

Prefrontal cortex and basal ganglia (plan and design movements); primary motor area and area 4 (make movement happen)

360

Corticospinal tracts are the effector pathways for _____ movements; whilst the cortico-reticulo and tubro-spinal tracts and the effectors for _____ movements

Skilled; global

361

What is the net effect of the direct vs indirect basal ganglia pathway?

Direct = increase in muscle acitivty; Indirect = suppression of muscle activity

362

In the direct basal ganglia pathway, inputs from the entire cortex pass onto what sort of neurons in the neostriatum?

Medium spiny neurons (MSN)

363

Neurons from which basal gangli are tonically inibiting the thalamus under normal conditions?

Globus pallidus internus and substantianigra pars reticularis

364

Subthalamic nuclei activation promotes diffuse generalised activation in which other basal ganglia structures?

Globus pallidus internus and substantianigra pars reticularis

365

Pedunculo-pointine reticular formation has profound influences on which functions? Via which tracts? Where do these tracts terminate?

Locomotion and posture; reticulospinal tracts; all levels of the spinal cord

366

List 3 functions (aside from posture and locomotion) that are influenced by the pedunculo-pontine reticular formation

Respiration, cardiovascular and GIT activity

367

The medial component of the pedunculo-pontine reticular formation facilitates ____ muscles, whilst the lateral components releases _____ from reflex control

Extensor; extensor/antigravity muscles

368

Which NTs are abundant in the pedunculo-pontine reticular formation?

Excitatory - ACh and Glutamate

369

Which chromosome is damaged in Huntingtons, and how does this contribute to the disease process?

4; causes GABAergic cell death in the neostriatum (brakes applied harder to subthalamic nucleus, reduces basal inhibition on thalamus and results in execution of otherwise suppressed motor behaviours

370

How does Huntingtons lead to dementia?

Eventual retrograde loss of cortical neurons because striatal targets die