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week 8 Flashcards

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1
Q

Auditory Pathways Unconscious pathways

A

To the Superior Colliculus BRAINSTEM (midbrain)
- orient to sound
To the Reticular Formation BRAINSTEM (medulla, pons, midbrain - arouse to sound

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2
Q

Auditory Pathways
Conscious Hearing

A

Information travels upwards via Lateral Lemniscus in the brainstem to the Inferior Colliculus
Lateral Lemniscus = main ascending auditory
tract
From MGB (in thalamus) neurons project to the
primary auditory cortex in a bundle of fibres called Auditory Radiation

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3
Q

Three cortical areas are dedicated to processing
auditory information:

A
  • Primary auditory cortex is the site of conscious
    awareness of the intensity of sounds.
  • Secondary auditory cortex - compares sounds
    with memories of other sounds, then categorises
    the sounds as language, music, or noise
  • Wernicke’s area is where comprehension of
    spoken language occurs.
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4
Q

Conductive Hearing Loss (CHL)

A

disorders of the external ear (eg canal blocked by
cerumen/wax) or middle ear – sound air waves not able to transmit to the inner ear

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5
Q

Sensorineural Hearing Loss (SNHL)

A

disorders of the inner ear (haircells included), cochlear nerve, or central connections

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6
Q

Mixed hearing loss (MHL)

A

can also occur - mix of both CHL and SNHL

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7
Q

Weber Test

A

vibrating tuning fork on middle of forehead and asked to localize the sound
* Normal = sound is perceived equal in both ears

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8
Q

Rinne Test

A

vibrating tuning fork on bone behind patient’s ear and asked when sound fades out, then move the still vibrating fork to EAM and see if sound is heard again
* Normal/positive test = sound will be heard again at the EAM as air conduction better than bone conduction

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9
Q

Otitis Media (with effusion) occurs where and with what

A

middle ear infection (with fluid/swelling)

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10
Q

Otosclerosis

A

– fusion of the ossicles due to abnormal bony overgrowth

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11
Q

Presbycusis

A

the loss of high-frequency hearing with age

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12
Q

Acoustic Neuroma

A

(Schwannoma)– a benign tumour of Schwann cells of the CN 8, one of the early symptoms of irritation of the nerve fibres can be tinnitus (‘ringing’ in the ear) eventually the ear becomes deaf

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13
Q

Meniere’s disease: (hearing impairment)

A

Affects the whole labyrinth – usually from increased endolymph in membranous labyrinth
Intermittent hearing loss/changes (including tinnitus) as well as symptoms related to
vestibular system – vertigo, nausea, vomiting, nystagmus
Occurs in clusters of ‘attacks’ or regularly. Each attack lasting minutes or hours.

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14
Q

Cortical Deafness

A

extremely rare form of sensorineural hearing loss – BILATERAL damage to the primary auditory cortex and secondary auditory cortex (no apparent damage to structures of ear) - most often caused by stroke but also head injury or birth defect.

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15
Q

Auditory Agnosia

A

– destruction secondary auditory cortex usually spares ability to perceive sound but cannot ‘recognise’ sounds. Speech recognition also affected if it is the left secondary auditory cortex which is damaged

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16
Q

Auditory Verbal Agnosia –

A

pure word ‘deafness’ – inability to comprehend speech at all and cannot repeat (speech is heard as meaningless noise)

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17
Q

Conductive Hearing Loss (treatment)

A

clear out wax, treat infection tube to help persistent fluid drain (grommets), and other various surgical options,

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18
Q

HEARING AIDs - treatment

A

amplify the airwave signals to help them be detected by damaged ears - can be helpful for some types of mild to moderate SNHL (and/or CHL)

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19
Q

Why is the vestibular system important?

A

Provides conscious perception of
Has an essential role in two areas of motor function
And has a role in autonomic function and consciousness

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20
Q

Hair Cells within the Vestibular Labyrinth
TRANSDUCTION

A

converting tilt, acceleration, and velocity into neural signals
Mechanical deformation of stereocilia and the kinocilium (unique to vestibular system) causes depolarisation of hair cell:
→ release of neurotransmitter
→ action potential in the vestibular portion of CN8

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21
Q

Utricle and Saccule os housed where and detects what

A

vestibule
→ linear acceleration/deceleration and tilt of head with respect to gravity

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22
Q

Cristae Ampullaris is housed where and detects what

A

within the ampulla of each semicircular canal
→ rotational acceleration of the head

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23
Q

Maculae

A

are the receptors within these otolith organs – epithelium of hair cells, topped by gelatinous material covered with otoconia/otoliths

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24
Q

Macula utriculi

A
  • HORIZONTAL orientation
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25
Macula sacculi
VERTICAL orientation
26
Semicircular Canals
3 fluid filled rings arranged perpendicular to each other
27
Semicircular Canals role
Role: respond to →rotational acceleration/deceleration the head (Change in velocity)
28
what is the sensory organ within the semicircular canals
Crista Ampullaris
29
Reciprocal action
increased signal from one canal occurs simultaneously with decrease signal from its partner Signal increases on side head is turning towards.
30
Perception of head orientation occurs in which pathway
Vestibulothalamocortical pathway
31
Vestibulooccular
via MLF to CN nuclei 3,4,6
32
Vestibulospinal
Medial and Lateral VS Tracts
33
Vestibulocerebellar
direct and via lateral vestibular nuclei - paths shown in the small diagram
34
Sensory Weighting model
* how much importance or ‘weight’ is attached to each sensory input at any one time * for example, balancing with eyes closed ‘weights’ the proprioceptive system and vestibular system
35
Integration of sensorimotor system
* sensorimotor system integrates afferent, efferent inputs in central nervous system, and is controlled by * two control systems: feedback control and feedforward control.
36
Feedforward control
is described as an anticipatory action with a direct descending command (plan to push a heavy door)
37
Feedback control
the cerebellar system regulates the visual, vestibular and somatosensory inputs during the activity. Feedback is conveyed to the cortex to be processed, and the reactive motor command is sent to muscles (door is lighter than expected, reactive changes to our posture)
38
Vertigo
conscious illusion of the world (or themselves) spinning or moving , feel as though swaying or tilting
39
Nystagmus
rapid, rhythmic repetitive oscillatory involuntary eye movements
40
Oscillopsia
lack of gaze stabilisation makes vision ‘jumpy’ /blurry
41
Lateropulsion
– gait leaning or turning to one side (usually fall towards side of peripheral lesion)
42
Gait ataxia
clumsy, poorly controlled voluntary movements
43
Vertigo caused by
sudden imbalance of vestibular signals due to lesion anywhere along vestibular pathway
44
Imbalance/ataxia
* Incoordination; “without order” * balance disorder * difficulty maintaining orientation and control of posture * May involve veering
45
Vertigo Projections from the vestibular nuclei and symptoms of dysfunction:
* Sensory information about head movement and head position relative to gravity Vestibulothalamocortical paths
45
Nystagmus Projections from the vestibular nuclei and symptoms of dysfunction:
Gaze stabilization – eye movement control - Medial Longitudinal Fasciculus Vestibuloocular paths – pathologica
46
– Unsteadiness/leaning Projections from the vestibular nuclei and symptoms of dysfunction:
Postural adjustments – postural control – sends messages to Lower Motor Neurons of antigravity muscles Vestibulospinal paths (medial and lateral)
47
ataxic’ movements of eyes -> double vision Projections from the vestibular nuclei and symptoms of dysfunction:
* Control of amplitude of muscle response Vestibulocerebellar
48
Nausea, sweating, anxiety Projections from the vestibular nuclei and symptoms of dysfunction:
* Autonomic function and consciousness – info sent to reticular formation Vestibuloreticular
49
Saccadeseye movement
rapid, ballistic movements – abruptly change point of fixation, voluntary or reflexive
50
Smooth Pursuit eye movement
slower, tracking movements, voluntary control
51
Vergence eye movement
aligns both eyes fovea with objects at varying distances (Disconjugate)
52
* Vestibulo-ocular eye movement
stabilize the eyes relative to the external world, most effective with rapid head movements
53
Vestibular Ocular Reflex role
To stabilize visual images on the retina (gaze stability) during head movements ACTIVATED BY (VESTIBULAR INPUT) HEAD MOVEMENT Works to prevent our visual word from bouncing/jumping around whenever we move
54
Vestibular Ocular Reflex Mechanism
As head turns, signals from the SC canals are relayed to the vestibular nuclei and onward along the pathway to exert extraocular muscle control.
55
Physiological nystagmus is an example of this ‘jerk’ Nystagmus is
the commonly seen type with a slow ‘drift’ and quick ‘catch up’ saccade type (back to the primary central position).
56
Optokinetic Reflex
Eyes follow a moving scene – visual stimulus is the cause * Smooth pursuit movements to keep the image stationary on the retina * Once reach their end of range eye jump back to the start with a Saccade * Alternating smooth pursuit and saccadic movements are seen
57
Benign Paroxysmal Positional Vertigo
* Otoconia dislodge and float from the maculae into the canals * Cupula makes a ‘dead-end’ in the canals (dislodged crystals can’t float out of canal) * Posterior Semicircular Canal most often affected * Symptoms arise due to otoconia falling to new position during head movements. * Abnormal flow of endolymph in the canal creates abnormal CN8 signals * Mismatch between the paired canals causes vertigo
58
Meniere’s Disease
swelling of the membranous labyrinth (see auditory lecture) – usually ONE ear but can be both
59
Other Unilateral Vestibular Loss (UVL)
eg. - Acute Vestibular Neuritis – Inflammation of the vestibular nerve, no hearing loss - Vestibular Labyrinthitis – Inflammation of the labyrinth – has associated hearing changes
60
Vestibular Schwannoma
benign, slow growing tumour of vestibular nerve (brain tumour)
61
Central Vestibular Dysfunction
Central Vertigo – sensation of motion despite being still * Ischaemic Stroke Posterior Fossa * Hemorrhagic stroke of brainstem or cerebellum, vestibular tracts * Trauma – Acquired Brain Injury, Concussion * Multiple Sclerosis * Migraine
62
Disorders of olfaction
*Loss of smell = anosmia *Decreased sensitivity to odorants = hyposmia or olfactory hypesthesia
63
Causes of anosmia or hyposmia
Upper respiratory tract infections Head trauma – shearing of olfactory bulb relative to cribriform plate Brain tumour – neuroblastomas and meningiomas may compress cranial nerves Smoking Age related & neurodegenerative disorders (e.g. PD & Alzheimer's disease)
64
How might anosmia or hyposmia affect function?
Smell is associated with taste – if unable to smell may lose interest in eating May be unable to detect gas leaks, smoke, spoiled food
65
Assessment of olfaction
Cranial Nerve 1 Standardised Smell Identification Tests eg University of Pennsylvania Smell test (UPSIT) – scratch and sniff test
66
Neural structures associated with taste
Receptor cells in the papillae Cranial nerves VII, IX and X synapse in the Solitary nucleus in the brainstem Synapse in the Ventral posteromedial thalamus Terminates in the Gustatory Cortex
67
Function of taste
Taste system + olfactory + trigeminal chemoreceptive system = is food safe to be ingested?
68
Causes of loss of taste
Ageing Head trauma Upper respiratory and Sinus infections Covid-19 Radiation therapy in the area
69
Ageusia
Loss of taste
70
Changes to function associated with impairment of taste
Taste, smell and appearance of food will influence food choices Sensory stimuli act as triggers to initiate and modulate digestion Complete or partial loss of taste or smell may result in loss of appetite
71
Assessment of taste
Tests *Drops placed on tongue person has to identify taste *Taste tablets *Taste strips Functional MRI (Research) *To highlight the areas of the brain involved in the gustatory pathway
72
Role of vision in function
* Arm function such as reaching, grasping and manipulating objects, walkingcand mobility * Analysis of the environment and guiding movement – obstacle negotiation, road crossing, Driving * Maintaining balance * Perceiving depth * Face and object recognition * Reading
73
Major structures of the eye - Accessory Structures
* Eyelids * Eyelashes * Lacrimal apparatus (for production, secretion & removal of tears)
74
where is the retina
ath back of the eyeball
75
Nerve innervation of extraocular eye muscles
*Superior Oblique = CN IV, LR =CN VI, all the rest = CN III
76
Eyeball moved by:
*4 rectus muscles o Superior rectus o Inferior rectus o Medial rectus o Lateral rectus *2 oblique muscles o Superior oblique o Inferior oblique
77
Clinical assessment of vision, eye movements and reflexes
* Visual fields* * Eye Movements - nystagmus, smooth pursuit*, vergence and saccadic eye movements * Pupillary light reflex * Acuity test * Ocular movement * Visual field screening test
78
rods
see low light, not colour
79
cones
see high light, colour
80
Fovea
Centre of macula, highest concentration of cones, site of sharpest vision
81
Blindness
occurs in one eye, a complete block to the visual field
82
Bitemporal hemianopia
opposite half of side of both eye of vision is loss eg left side of left eye and right side of right eye
83
Homonymous hemianopia
half of side of both eye of vision is loss eg both right side of both eyes loss vision
84
Quadrantanopia
a quater of both eyes loss vision
84
Pupillary light reflex
eflexive response where both pupils constrict in response to the bright light.
85
dyskineasia cp
involuntary and fluctuating muscle movements, abnormal postures, and difficulty with voluntary motor control
86
spactic cp
the most common type of cerebral palsy. The muscles of people with spastic cerebral palsy feel stiff and their movements may look stiff and jerky.

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