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BRS missed out > Neurology missed out questions > Flashcards

Neurology missed out questions Flashcards

1
Q

How is the cortex organised microscopically?

A
  • rganised into layers and columns
  • 6 layers (I most superficial and VI most deep) and multiple cortical columns
    I - molecular layer
    II -External Granular layer
    III- External Pyramidal LAyer
    IV- INternal granular layer
    V- INternal pyramidal layer
    VI- multiform layer
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2
Q

What is the cytoarchitecture of the cortex?

A

Cytoarchitecture is cell size, spacing or packing density and layers

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3
Q

How many areas was the brain divided into according to Brodmann?

A

52

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4
Q

Which aspects of the brain divided according to cytoarchitecture corresponds to the primary somatosensory and motor region?

A

primary somatosensory (1, 2, 3) and primary motor (4)

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5
Q

What is the limbic lobe made up of?

A
  • Amygdala
  • Hippocampus
  • Mamillary body
  • Cingulate gyrus
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6
Q

What functions is the limbic lobe responsible for? (5)

A
  • Learning
  • Memory
  • Emotion
  • Motivation
  • Reward
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7
Q

What is the insular cortex and what’s its function?

A
  • visceral sensations
  • autonomic control and interoception
  • auditory processing
  • visual-vestibular integration
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8
Q

what types of white matter tracts are there?

A
  • Association fibres-
    Commissural fibres
  • Projection fibres
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9
Q

Association fibres- what do theses do?

A

Connect areas within the same hemisphere- there are short and long fibres

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10
Q

What fibres connect Frontal and occipital lobes ?

A

Superior longitudinal fasciculus

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11
Q

What fibres connect Frontal and temporal lobes ?

A

Arcuate fasciculus

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12
Q

What fibres connect Temporal and occipital lobes

A

Inferior longitudinal fasciculus

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13
Q

What fibres connect Frontal and temporal lobes ?

A

UNcinate fasciculus

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14
Q

Commissural fibres- what do these do and give two examples?

A
  • Same structure different hemispheres
    Corpus callosum (can be disconnected in patients with epilepsy to treat it)
  • Anterior commissure
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15
Q

How do deeper fibres radiate through the cortex? And what do they converge through?

A

Corona radiata
Internal capsule

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16
Q

What do the primary/secondary cortices in the motor area of frontal lobe do

A
  • Primary motor cortex- controls fine, discrete, precise voluntary movements and provides descending signals to execute movements
  • Premotor area- involved in planning movements (e.g. externally cued like seeing and wanting to pick up an object)
  • Supplementary area- involved in planning complex movements (e.g. internally cued like production of speech)
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17
Q

Prefrontal cortex- what it do?

A
  • Adjusting social behaviour
  • Personality expression
  • Attention
  • Planning
  • Decision making
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18
Q

What do parietal lobe lesions do?

A
  • Contralateral neglect (if right sided lesion)
    • Lack of awareness of self on left side
    • Lack of awareness of left side of extrapersonal space
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19
Q

What do temporal lobe lesions do?

A

Leads to agnosia- inability to recognise
Anterograde amnesia

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20
Q

What does a lesion to the arcuate fasciculus cause?

A

Conduction aphasia- inability to repeat speech (this tract links the Broca’s area and Wernicke’s area)

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21
Q

What does positron emission tomography (PET) do?

A

Looks at blood flow directly to a brain region by seeing how glucose (radioactive isotope used) is taken up by different parts of brain

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22
Q

What is diffusion tensor imaging (DTI)?

A

Based on diffusion of water molecules

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23
Q

How are somatosensory evoked potentials measured?

A
  • We can see a series of waves that reflect sequential activation of neural structures along the somatosensory pathways (see diagram and order of waves)
    • We can put electrodes along a certain neural pathway and see if there are any issues
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24
Q

What is TMS?

A

transcranial magnetic stimulation
- Uses electromagnetic induction to stimulate neurones
- assess functional integrity of neural circuits

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25
Q

What is transcranial direct current stimulation (tDCS)?

A

Uses low direct current over the scalp to increase or decrease neuronal firing rates

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26
Q

describe what M-waves, F-waves and H reflexes are and what information they can provide.

A

M waves - this is when you stimulate the motor axon, it is quick but doesn’t have enough energy to build up
F waves- This is the rebound information, when the mototr axon is stimulated but it goes backwards and rebounds to the start
H reflexes - this is when the sensory neurones is stimulated and the reflex arc is started and mototr activity starts up because of that.

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27
Q

IN an F - wave A large electrical stimulus can cause activation of the motor axons to conduct ——-

A

antidromically

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28
Q

Total motor conduction time (TMCT)

A

time from brain to muscle (MEP latency)

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29
Q

Peripheral motor conduction time (PMCT) –

A

time from spinal cord to muscle along motor axon

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30
Q

Peripheral motor conduction time (PMCT) – time from spinal cord to muscle along motor axon can be calculated using the formula:

A

PMCT = (M latency + F latency-1) /2

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31
Q

Central motor conduction time (CMCT) is therefore

A

TMCT - PMCT

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32
Q

Describe the hierarchal organisation of the brain

A

High order areas of hierarchy is involved in more complex such as planning movements and the coordination tips of muscle activity, while low orders are involved in the execution of

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33
Q

Describe the hierarchal organisation of the brain

A

High order areas of hierarchy is involved in more complex such as planning movements and the coordination tips of muscle activity, while low orders are involved in the execution

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34
Q

Describe the functional segregation of motor control

A

Motor systems organised in a number of different areas that control different aspect of movemt

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35
Q

What are the pyramidal tracts and name them

A

They pass through the pyramids of the medulla
Corticospinal, corticobulbar
Voluntary movement of body and face
From motor cortex to spinal cord/ cranial nerve

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36
Q

What are the extrapyramidal tracts and name them

A

Do not pass through the pyramids of the medulla:

Vestibulospinal, Tectospinal, Reticulospinal, Rubrospinal

Brainstem nuclei to spinal cord
Involuntary, movement for balance , posture and locomotion

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37
Q

Describe the corticospinal tracts , what it passes through and its function

A

There are the lateral and anterior corticospinal tract
Upper motor neuron —> cerebral peduncle (between cerebrum and brain stem) —> Medulla (decussates - lateral) —> Lower motor neuron
Anterior corticospinal uncrossed fibre : trunk muscles
Lateral corticospinal crossed fibres : limb muscle

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38
Q

What does the motor homunculus show?

A

How much of the brain is devoted to that region

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39
Q

What does somatotopic representation show?

A

From, Where each region of the motor cortex innevrates the muscle

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40
Q

What do motor nerves from each of these nuclei do?
Oculomotor nucleus
Trochlear nucleus
Trigeminal motor nucleus
Abducens nucleus
Facial nucleus
Hypoglossal nucleus

A

Eye
Eye
Jaw
Eye
Face
Tongue

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41
Q

Name the extra pyramidal tracts and describe their function

A

Vestibulospinal - stabilise head during body movement, coordinate head movement with eye movement, mediate postural adjustment
Reticulospinal - changes in muscle tone associated with voluntary movements, postural stability
Tectospinal- from superior colliculus of midbrain , orientation of head and nexk during eye movement
Rubrospinal - from red nucleus of midbrain, inner age lower motor neurons of flexors of upper limb not as relevant in humans

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42
Q

Upper motor neuron lesion positive signs

A

Increased abnormal motor function due to loss of inhibitory descending inputs
Spasticity
Hyper reflexia
Clonus
Babinksi sign (extensor plantar responses)

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43
Q

Upper motor neuron lesion negative signs

A

Loss of voluntary motor function (flexors stronger than extensors UL and extensors stronger than flexors in LL)
Paresis
Paralysis

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44
Q

Apraxia - description and cause

A

Disorder of skilled movement, not paretic but has lost information on how to do it
Lesion of inferior parietal lobe , the frontal lobe
Typically caused by stoke or dementia

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45
Q

Lower motor lesion symptoms

A

Weakness, Hypotonia, Hyporeflexia, Muscle atrophy, Fasciculations, Fibrillations (EMG)

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46
Q

Motor neuron disease is also known as

A

AMYOTROPHIC LATERAL SCLEROSIS

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47
Q

Symptoms of motor neuron disease upper motor signs

A

Spasticity
Brisk limbs and jaw reflexes
Babinskis sign
Loss of dexterity
Dysarthria
Dysphagia

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48
Q

Symptoms of motor neuron disease lower motor symptoms

A

Weakness, muscle wasting, tongue fasciculations , nasal speech, dysphagia

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49
Q

Structure and function of parts of the basal ganglia ( 4)

A

Caudate nucleus - decision to move
Lentiform nucleus ( putamen + external globus pallidus) - elaborated associated movement ( swinging arms while walking, facial expression to match emotions)
Substantia nigra ( midbrain) - Moderating and coordinating movement ( suppressing unwanted movement )
Ventral pallidum - Performing movement in order

Striatum - caudate and putamen

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50
Q

Parkinson disease - pathology and symptoms

A

Degeneration of the dopaminergic neurons that originate in substantial nigra and project to striatum

Bradykinesia
Hypomimic
Akinesia
Rigidity
Tremor at rest

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51
Q

Huntington disease- pathophysiology and symptoms

A

CAG repeat, autosomal dominant

Degeneration of GABAergic neurons in the striatum, caudate and then putamen

Choreic movement
Rapid jerky movement - hands and face first then legs then rest of body
Speech impairment
Dysphagia
Unsteady gait
Cognitive decline + dementia

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52
Q

Ballism- cause and symptom

A

Stroke affecting subthalamic nucleus

Sudden uncontrollable flinging of extremities
Symptoms contralateral

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53
Q

Cerebellum
Location
Separated by cerebrum by
Function

A

Posterior cranial fossa
tentorium cerebelli
Coordinator and predictor of movement

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54
Q

Three cerebellar diseases

A

Disease of Vestibulocerebellum
Disease of spinocerebellum
Disease of cerebrocerebellum

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55
Q

What is the function of the vestibulocerebellum

A

Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements

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56
Q

Lesion of the vestibulocerebellum

A

Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)

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57
Q

Function of the spinocerebellum

A

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements

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58
Q

Lesion of the spinocerebellum

A

Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)

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59
Q

Functon of the cerebrocerebellum

A

Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control

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60
Q

Lesion of the cerebrocerebellum

A

Damage affects mainly arms/skilled coordinated movements (tremor) and speech

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61
Q

Main signs of cerebellar disease ( appaerant only on movement)

A

Ataxia
-General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait

Dysmetria
-Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)

Intention tremor
-Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)

Dysdiadochokinesia
-Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)

Scanning speech
Staccato, due to impaired coordination of speech muscles

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62
Q

Alpha motor neuron
- what are they?
- what do they innervate?
-what does activation cause?
-what are all alpha neurons that innervate a single muscle collectively known as?

A
  1. Lower motor neurons of brain stem and spinal cord
  2. Extrafusal fibres of skeletal muscle
  3. Contraction of muscle
  4. Motor neuron pool
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63
Q

Motor unit

A

a single neuron and all the muscle fibres it innervates

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64
Q

Slow (S) vs Fast, fatigue resistant ( Type IIa) vs Fast fatiguable ( Type IIb)

A

Diameter - Increases in diameter
Dendritic tree - Gets larger
Axon - Gets thicker
Conduction velocity - Gets faster
Force generated - Gets larger

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65
Q

What are the three different types of motor units characterised by?

A

amount of tension generated
speed of contraction
fatiguability.

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66
Q

Describe the two mechanisms of force generation

A

Recruitment - the smallest motor units are recruited first, allows for fine control,

Rate coding - the frequency of firing elicits greater force generation. If no time between firing; summation

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67
Q

Role of neurotrophic factors

A

Prevent neuronal death

Promote growth of neurons after injury

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68
Q

What are common states that lead to changes in muscle fibre properties. (Plasticity)

A

Training - Type IIb to IIa
Severe deconditioning or spinal cord injury - Type I to II
Ageing - Loss of type I and II but preferential loss of type II

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69
Q

Describe Jendrassik manoeuvre

A

clenching the teeth, making a fist, or pulling against locked fingers - Makes reflex larger

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70
Q

What is seen in hyper- reflexia?

A

Loss of descending inhibition
Associated with upper motor neuron lesions
Overactive reflexes

Involuntary and rhythmic muscle contractions - Clonus

Curls upwards following blunt along sole of foot – positive Babinski sign.

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71
Q

What is seen in hypo reflexia?

A

Below normal or absent reflexes
Associated with lower motor neuron diseases

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72
Q

What is a hallmark of pure corticospinal lesion?

A

Absent abdominal reflex with others present

73
Q

How are headaches classified according to international headache society?

A

Primary or Secondary Headache

74
Q

Primary vs Secondary Headache syndromes

A

Primary:
Migraine, Tension-type headache ,Trigeminal autonomic cephalalgias, Cluster headache

Secondary:
Headache is spercipitated by another condition / disorder - local os systemic.

75
Q

How would you further categories primary headaches?

A

Long lasting >4 hrs
Migraine
Tension type headache
Medication overuse headache

Short lasting < 4 hours
Cluster headache
Trigeminal autonomic cephalalgias

76
Q

Red flag symptoms of headaches

A

Age - new onset or diffeent headahce in >50 years old
Onset - sudden abrupt onset of severe headache ( thunderclap)
Systemic symptoms - fever, necl stiffness, rash, weight loss
Neurological signs -Confusion, impaired consciousness, focal neurology, swollen optic discs

77
Q

Central hypothesis pathology : MIgraine

A

Headache pain is caused by the activation of the trigeminovascular system (TGVS)

The tgvs also causes central sensilitization which increases headache pain.

The TGVS also causes vasodilation and neurogenic inflammation via calitonin gene related peptide ( cgrp). This further actovates TGVS

The TGVS is activated by abnormal brain stem function and cortical spreading depression. Cortical spreading depression also causes the migraine ‘aura’. Cortical spreading depression is caused by abnormal cortex hyperexcitability

78
Q

Characteristics of a migraine

A

Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by routine physical activity
Last hours and sometimes days

Usually one or more of:
Nausa and/or vomiting
photophobia and/or phonophobia
aura

79
Q

Features of auras ‘migraine’

A

Expanding ‘C’s
Elemental visual disturbance
Gradual evolution: 5-30minutes (<60minutes)
Usually before headache

80
Q

MIgraine phases

A

Premonitory: yawning, polyuria, mood change, irritable, light sensitive, neck pain, concentration difficulty

Aura: Visual, sensory (numbness/paraesthesia), weakness, speech arrest

Headache: Head and body pain, nausea, photophobia

Resolution: rest and sleep

Recovery: mood disturbed, food intolerance, feeling hungover

Can take up to 48 hours

81
Q

Migraine management:

A

Lifestyle - avoid triggers, diet, sleep, exercise, mindfulness

Pharmacological therapy -
Acute/ Abortive : Paracetamol, NSAIDs, Prokinetics, Triptans

Long term/ Preventative :
>5 days/month
“low and slow” with doses until at optimal dose

82
Q

Migraine preventatives

A

ACE inhibitors
Angiotensin II blockers
Serotonin antagonists
B blockers
Anti convulsants
Anti depressents
Parenteral

83
Q

Characteristics of tension type headache

A

Tight muscles around head and neck, as though head is in a vice.

Lasts 30mins (but can be hours long):
Bilateral
Mild or moderate
Not aggravated by movement
No added features typically
No nausea or vomiting
No photophobia or phonophobia

84
Q

Treatment of tension type headache

A

Reassurance
Paracetamol

85
Q

Cluster headache characteristics

A

Severe unilateral pain
Last 15-180 minutes if untreated.

At least one of the following, ipsilaterally:
Conjunctival redness and/or lacrimation
Nasal congestion and/or rhinorrhoea
Eyelid oedema

Forehead and facial sweating
Miosis and/or ptosis
A sense of restlessness or agitation
Not associated with a brain lesion on MRI

86
Q

Cluster headache management

A

Acute
Triptan. Nasal or subcutaneous route
High flow oxygen. Oxygen inhibits neuronal activation in the trigeminocervical complex

Prevention
Verapamil (Calcium channel inhibitor)
Get an ECG first!
Greater occipital nerve block

87
Q

What is the function of a) vestibular and b) hearing organ?

A

a) capture low frequency - movement
b) capture high frequency - sound

88
Q

Evolution of the vestibular sensory division

A

Statocyst –> Utriculus –> Sacculus –> a) Cochlea , Canals

89
Q

Frequency measured in BLANK describes what we call BLANK and is

A

Hertz
Pitch
Cycles per second, perceived tone.

90
Q

Amplitude measured in BLANK describes what we call BLANK and is

A

dB
Loudness
Sound pressure, subjective attribute correlated with physical strength.

91
Q

Human range of hearing

A

Frequency: 20–20,000Hz

Loudness: 0 dB to 120 dB sound pressure level (SPL)

92
Q

Outer ear function

A

CAPTURE & FOCUS SOUND: To capture sound and to focus it to the tympanic membrane.

PROTECTION: To protect the ear from external threats.

AMPLIFICATION: Modest amplification (10DB) of upper range of speech frequencies by resonance in the canal.

93
Q

Function of the Middle Ear

A

AMPLIFICATION: The main function of the middle ear is mechanical amplification (can provide an additional 20-30dB)

94
Q

Function of the Inner Ear aka cochlea

A

TRANSDUCTION- transduce vibration into nervous impulses

CAPTURE SOUND - captures the frequency (or pitch) and intensity (or loudness) of the sound

95
Q

3 compartments of the cochlea

A

Scala vestibuli and scala tympani: Bone structures, contain perilymph (high in sodium)

Scala media: Membranous structure, contains endolymph (high in potassium). Here is where the hearing organ or Organ of Corti is located.

96
Q

Basilar membrane where the structure Organ of Corti ies is arranged

A

tonotopically,

97
Q

The organ of Corti contains two types of hair cells

A

Inner hair cells (IHC) and

Outer hair cells (OHC)

98
Q

Tectorial membrane
location and function

A

above the hair cells and allows hair deflection, which in turn will depolarise the cell.

99
Q

Inner hair cells (IHC) function

A

carry 95% of the afferent information of the auditory nerve. Their function is the transduction of the sound into nerve impulses

100
Q

Outer hair cells (OHC) function

A

carry 95% of efferents of the auditory nerve. Their function is modulation of the sensitivity of the response.

101
Q

The hairs of the hair cells are called

A

stereocilia.

102
Q

Explain transduction of sound in the ear

A

The deflection of the stereocilia towards the longest cilium (kinocilium) will open K+ channels

This depolarises the cell releasing the neurotransmitter to the afferent nerve which then depolarises.

103
Q

How will louder sounds be affect transduction

A

Higher amplitudes (louder) of sound will cause greater deflection of stereocilia and K+ channel opening

104
Q

Auditory pathways

A

Spiral ganglions via the vestibulo-cochlear nerve (8th Cranial nerve) travel to the ipsilateral cochlear nuclei (monoaural neurons) in the brainstem (pons)

Auditory information crosses at the superior olive level

After this point all connections are bilateral

105
Q

Types of hearing loss - broad category

A

Anatomical

106
Q

Anatomical hearing loss

A

Conductive hearing loss: Problem is located in outer or middle ear.

Sensorineural hearing loss: The sensory organ (cochlear) or the nerve (auditory nerve). (90% of all hearing loss!)

Central hearing loss: Very rare and originates in the brain and brainstem

107
Q

Timing of hearing loss

A

Sudden hearing loss minutes to days

Progressive hearing loss months to years

108
Q

Causes of condusive hearing loss

A

Outer ear - foreign body, wax
Middle ear - Otitis ( seen by bubbles that suggest fluid in ear) , Otoscleorosis

109
Q

Causes of sensorineural hearing loss

A

Inner ear - Noise, Presbycusis, Ototoxicity

Nerve - acoustic neuroma (vestibular schwannoma) (unilateral)

110
Q

Two tests for hearing bedside

A

Weber test - tuning fork over head

Rinne test - tuning fork behind ear

111
Q

WHat is audiometry and what is the difference between conductive and sensironeural

A

The audiogram is where the hearing thresholds are plotted to define if there is a hearing loss or not. A normal hearing threshold is located between 0 – 20dB

Consistently lower than normal for condusive but for sensironeural it is low at higher frequencies

112
Q

Special tests for hearing - Otoacoustic Emissions (OAEs)

A

This test is often part of the newborn hearing screening and hearing loss monitoring.

Low-intensity sounds called OAEs

These sounds are produced specifically by the outer hair cells as they expand and contract

113
Q

Treatment for hearing loss

A

UNderlying cause

Brainstem implants

Hearing aids

Cochlear implants

114
Q

What makes up the vestibular systems?

What is the input, what is the output?

A

Mechanical sensors (canals and otoliths)

Input: Movement and gravity
Output: Ocular reflex, Postural control

115
Q

How many semicircular cannals are there, describe them ?

A

Three - anterior, posterior and lateral

They have ampulla on one side, and they are connected to the utricle.

utricule and saccule are located in the vestibule and are joined by a conduit. The saccule is also joined to the cochlea

116
Q

What are the otolith organs?

A

Utricle and saccule are the otolith organs. Their cells are located on the maculae, placed horizontally in the utricle and vertically in the saccule

117
Q

What is the maculae in relation to the ololith organs?

A

The maculae contain the hair cells, a gelatinous matrix and the otoliths on top. These otholiths are carbonate crystals that help the deflection of the hairs.

118
Q

What leads to otolith movement

A

Linear acceleration and tilt: otolith movement
Utricule: horizontal movement

Saccule: vertical movement

119
Q

What movement causes deflection towards the kinocilium

A

Head tilt backwards and acceleration

120
Q

What makes up the semicircular canal?

A

The hair cells in the canals are located in the ampulla.
The rest of the canal only has a liquid high in potassium called endolymph
The ampulla has the crista, where the hair cells are located. The cells are surrounded by the cupula which helps the hair cell movement

121
Q

Orientation of the canals in the head

A

The orientation of the canals in the head defines three planes.

Anterior and posterior canals form a 90° angle. Lateral canals are horizontal to the other canals.

Therefore they work in pairs

122
Q

Hair cell potential in vestibular movement

A

resting potential which has a basal discharge to the nerve

towards the kinocilium generates depolarization and an increase in nerve discharge

away from the kinocilium generates hyperpolarization and a reduction in nerve discharge

123
Q

Vestibular nerve and nuclei

A

Primary afferents end in vestibular nuclei in the brainstem (pons)

124
Q

Vestibular system functions

A

To detect and inform about head movements

To keep images fixed in the retina during head movements

Balance

125
Q

Vestibular reflexes

A

Vestibulo-ocular Reflex
(VOR)

Vestibulo Spinal Reflex
(VSR)

126
Q

Describe the Vestibulo-ocular reflex (VOR)

A

Keeps images fixed in the retina

Connection between vestibular nuclei and oculomotor nuclei

Eye movement in opposite direction to head movement, but same velocity and amplitude

127
Q

Vestibular disorder – how to categorise them

A

Timing

Laterality

128
Q

What are the main complaints in In acute AND unilateral vestibular disorders?

A

Main complaints - imbalance, dizziness, vértigo and nausea

129
Q

What are the main complaints In slow AND unilateral or any bilateral loss: vestibular disorders?

A

Main complaints – imbalance and nausea – NO vertigo

130
Q

Balance disorders: LOCATION

A

Peripheral vestibular disorders –> Vestibular organ and/or VIII nerve –> Vestibular neuritis
Benign Paroxysmal Positional Vertigo (BPPV)
Meniere’s disease

Central vestibular disorders –> CNS (brainstem/cerebellum) –> Stroke , Multiple Sclerosis , Tumours

131
Q

Clinical approach for a physician in acute vertigo:
The main diagnosis
The core exam

A

The main diagnoses
- BPPV
- Vestibular Neuritis
- Vestibular Migraine
- Stroke (cerebellar)

The core exam
EYES
EARS
LEGS

132
Q

Red Flags in vestibular disorders

A

Headache
Gait problems
Hyper-acute onset
Hearing loss
Prolonged symptoms (>4 days)

133
Q

Balance disorders: Timing (evolution)

A

Acute - Vestibular Neuritis , Stroke
(HINTS exam)

Intermittent - Benign Paroxysmal Positional Vertigo (BPPV)
Dix-Hallpike test

Recurrent - Migraine
(Meniere’s Disease)

Progressive - Schwannoma vestibular (VIIIth nerve)
Degenerative conditions (MS)

134
Q

HINTS exam – clinical exam in acute dizziness

A

To decide between :
Vestibular Neuritis or Stroke?

Head Impulse Test ​

Horizontal rotational VOR

Nystagmus​

Vestibular organ Vs Cerebellar/brainstem nystagmus

Test of Skew Deviation​

Vertical misalignment - usually absent in peripheral pathology

135
Q

What can be done to restore the crystals back in Benign Paroxysmal Positional Vertigo (BPPV)

A

Epley or Semont.

136
Q

What features can be seen in the MRI of a patient with Dementia?

A

AB
Neuronal tau
TDP 43
a- synuclein

137
Q

MMSE involves questions in which 6 categories?

What other examination could you do to confirm dementia?

A

Orientation, Registration, Attention and Calculation, Recall, Language, Copying

ACE III

138
Q

What is the scoring in MMSE

A

24-30 no cognitive impairment
18 -23 mild cognitive impairment
0- 17 severe cognitive impairment

139
Q

What bloods should you order in testing for dementia?

A

FBC, CRP, ESR, Thyroid function, Biochemistry and renal function, Glucose, B12 and folate, Clotting, Syphillis serology, HIV, Caeruloplasmin

140
Q

Management of dementia

A

Acetylcholinesterase inhibitors
Watch and Wait
Treating behavioural/ psychological symptoms
OT/ Social services
Specialist therapies

141
Q

Varients of dementia and features

A

Alzheimer’s - subtle , insidious amnestic/ non amnestic presentation, episodic memory loss

Vascular dementia - step wise deterioration +/- multiple infarcts

Dementia with lewy bodies - cognitive impairments before / within 1 year of Parkinsonian symptoms, visual hallucinations and fluctuating cognition, REM sleeping disorder

Frontotemporal dementia - behavioural variant FTD, semantic dementia, progressive non fluent aphasia

Rapidly progressing dementia

142
Q

Episodic memory

A

Memory for particular episodes in life

Dependent on the medial temporal lobes inc hippocampus

143
Q

Spatio - temporal evolution of amyloid and tau according to Thal and Braak

A

Amyloid - moves from superficial superior to deep inferior ( finally at brain stem)

tau - moves anterior to posterior

144
Q

How can amyloid be detected in vivo?

A

PET Amyloid

145
Q

Features of Alzheimers disease investigstions

A

Enlarged ventricles
Narrowed Gyri
Widened sulcus
Atrophy
Hippocampul atrophy
CSF - B amyloid plaque lower, Tau higher than controls

146
Q

Features of FTD investigations

A

Perisylvian volume decreased - asymmetric

Then genetic test

147
Q

Dementia with Lewy bodies investifations

A

DAT scan - dopamine presence

In caudate and Putamen in AD but decreased in DLB

148
Q

Inflammation terms define:
Meingitis

Myelitis

A

Inflammation of meninges- caused by infections, milky white autopsy in subarachnoid on autopsy

Inflammation of the spinal cord

149
Q

What forms the blood brain barrier?

A

BBB capillaries have extensive tight junctions at the endothelial cell-cell contacts, massively reducing solute and fluid leak across the capillary wall

150
Q

What happens following blood brain barrier dysfunction?

A

BBB gets compromised via stroke or physical trauma

This means fluids leak into brain including fibrinogen

Astrocytes react to presence of fibrinogen by withdrawing their end feet from the wall of the vessel, this further compromises the BBB

At the same time there’s a build up of collagen in the basement membrane which hardens the vessel wall and leads to small vessel disease

151
Q

Symptoms of encephalitis

A

Initially symptoms are flu-like with pyrexia (high body temperature) and headache

Subsequently, within hours, days or weeks:
confusion or disorientation
seizures or fits
changes in personality and behaviour
difficulty speaking
weakness or loss of movement
loss of consciousness

152
Q

Causes of encephalitis

A

Most cases encephalitis is caused by viral infection, the commonest of which are:

Herpes Simplex
Measles
Varicella (chickenpox)
Rubella (German measles)

others include; trauma, bacteria , autoimmune etc

153
Q

Treatment of encephalitis

A

Antivirals e.g. acyclovir
Steroids
Antibiotics/antifungals
Analgesics
Anti-convulsants
Ventilation

154
Q

Cellular pathology of MS

A

Inflammation
Demyelination
Axonal loss
Neurodegeneration

155
Q

Inflammation in MS caused by?

A

perivascular immune cell infiltration (CD3 T-cells and CD20 B-cells)

156
Q

Causes of Meningitis

A

Bacterial
Meningococcal – the most common cause of bacterial meningitis in UK
Streptococcal – the main cause in new-born babies

and other bacterial causes:
Pneumococcal
Haemophilus Influenzae type b (Hib)

Other causes
Viral - very rarely life-threatening
Fungal

157
Q

Symptoms of meningitis

A

sudden fever, severe headache, nausea or vomiting, double vision, drowsiness, sensitivity to bright light, and a stiff neck, rash (not always

158
Q

What diagnostic tests can be performed for meningitis? What might be found on these tests?

A

Neurological examination, CT, MRI, lumbar puncture (CSF is usually clear and colourless; low glucose in bacterial meningitis; raised white blood cell counts are a sign of inflammation), blood, urine analysis.

159
Q

What are the three layers of the eye and describe them

A

Sclera - hard and opaque, serves as protective outer coat , high water content
Uvea - composed of the Iris, ciliary body and choroid, pigmented and vascular,
Retina- neurosensory tissue , responsible for capturing the light rays that enter eye, sent to brain via optic nerve

160
Q

Optic nerve description

A

Transmits electrical impulses from the retina to the brain

Connects to the back of the eye near the macula

Visible portion is called the optic disc

161
Q

Macula description

A

Located roughly in the centre of the retina, temporal to the optic nerve

Small and highly sensitive part of retina responsible for detailed central vision e.g reading

Fovea is the very centre of the macula

162
Q

Where is the optic nerve blind spot?

A

Where the optic nerve meets the retina- there are no light sensitive cells

163
Q

Where is the optic nerve blind spot?

A

Where the optic nerve meets the retina- there are no light sensitive cells

164
Q

Central vision:
What part of vision does it participate in?
One part of the retina has a high concentration of a certain type of photoreceptors; which one?
How is it assessed?
What does the loss lead to?

A
  1. Detailed day vision, colour vision, reading, facial recognition
  2. Fovea had the highest concentration of cone photoreceptors
  3. Visual acuity assessment
  4. Poor visual acuity
165
Q

Peripheral vision:
What part of vision is it involved in?
How is it assessed?
What does loss lead to?

A
  1. Shape, movement, night vision, navigation vision
  2. Visual field assessment
  3. Unable to navigate in the environment
166
Q

What is the structure of the retina and what are their functions?

A

Outer layer- photoreceptors, detection of light

Middle layer- bipolar cells, local signal processing (contrast sensitivity)

Inner layer- retinal ganglion cells, transmission of signal from the eye to the brain

167
Q

Refraction - light from one medium to another change
How does the eye accommodate this?

A

Lenses- two types;
convex - converging lens takes light rays and brings them to a point
Concave- diverging lens take light rays and spreads them outward

168
Q

Emmetropia

Ametropia
Descriptions

A

Emmetropia- adequate correlation between axial length and refractive power, parallel light falls on retina

Ametropia - mismatch between axial length, refractive power

169
Q

Types of ametropia

A

Myopia- converge too early, caused by excessive long globe (axial) or excessive refractive power ( refractive), symptoms- blurred distance vision, headache

Hyperopia - converge too late, visual acuity at near tends to blur, asthenopic symptoms - eye pain, headache in frontal region, burning sensation in eyes

170
Q

Near response triad description

A

Pupillary Miosis (Sphincter Pupillae) to increase depth of field

Convergence (medial recti from both eyes) to align both eyes towards a near object

Accommodation (Circular Ciliary Muscle) to increase the refractive power of lens for near vision

171
Q

Presbyopia description and management

A

Naturally occurring loss of accommodation (focus for near objects)

Onset from age 40 years

Distant vision intact

Corrected by reading glasses (convex lenses) to increase refractive power of the eye

172
Q

Visual Pathway Landmarks

A

Eye

Optic Nerve – Ganglion Nerve Fibres

Optic Chiasm – Optic nerves from both eyes converge at the optic chiasm, 53% decussate to contralateral optic tract

Optic Tract – Ganglion nerve fibres continuation

Lateral Geniculate Nucleus (relay centre within thalamus) – Ganglion nerve fibres synapse

Optic Radiation – forms 4th order neuron, relay signal from the Lateral Geniculate Ganglion, to the Primary Visual Cortex

Primary Visual Cortex or Striate Cortex – within the Occipital Lobe, relays to extra-striate cortex (higher visual processing)

173
Q

Lesion at the optic chiasm description

A

Bitemporal hemianopia

174
Q

Lesion posterior to optic chiasm

A

Right sided lesion- left homonymous hemianopia in both eyes

Left sided lesion- right homonymous hemianopia in both eyes

175
Q

Optic chiasm uncrossed vs crossed fibres

A

Crossed fibres -Originate from nasal retina responsible for temporal visual field

Uncrossed fibres - originating from temporal retina, responsible for nasal visual field

176
Q

Homonymous hemianopia with macular sparing

A

damage to primary visual cortex as area representing macula recieves blood supply from posterior cerebral arteries both sides

Often due to stroke

177
Q

Pupillary reflex
where does pupil specific ganglion cells exit?

Describe the pathway

A

At the third postrior optic tract

Ganglion cells of axons project to pretectal region of midbrain
Synapse to Edinger–Westphal nucleus
Oculomotor nerve efferent would synapse at ciliary ganglion, will synapse with the short posterior ciliary nerve that innervates the pupillary sphincter and would lead to pulpillary contraction

178
Q

Afferent vs efferent defect seen through pupillary reflex assessment

A

Right afferent (damage to optic nerve)- when light shown in right side both eyes do not constrict but when left is stimulated they do

Right efferent (pupil constriction) - left eye constricts whether right or left eye shown with light but right eye doesn’t

179
Q

Swinging torch test (relative damage to afferent)

A

Both pupils constrict when light shown on undamaged side, but paradoxically both pupils dilate when light shown on damaged side

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