Neurology missed out questions Flashcards
(179 cards)
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
2
Q
What is the cytoarchitecture of the cortex?
A
Cytoarchitecture is cell size, spacing or packing density and layers
3
Q
How many areas was the brain divided into according to Brodmann?
A
52
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)
5
Q
What is the limbic lobe made up of?
A
- Amygdala
- Hippocampus
- Mamillary body
- Cingulate gyrus
6
Q
What functions is the limbic lobe responsible for? (5)
A
- Learning
- Memory
- Emotion
- Motivation
- Reward
7
Q
What is the insular cortex and what’s its function?
A
- visceral sensations
- autonomic control and interoception
- auditory processing
- visual-vestibular integration
8
Q
what types of white matter tracts are there?
A
- Association fibres-
Commissural fibres - Projection fibres
9
Q
Association fibres- what do theses do?
A
Connect areas within the same hemisphere- there are short and long fibres
10
Q
What fibres connect Frontal and occipital lobes ?
A
Superior longitudinal fasciculus
11
Q
What fibres connect Frontal and temporal lobes ?
A
Arcuate fasciculus
12
Q
What fibres connect Temporal and occipital lobes
A
Inferior longitudinal fasciculus
13
Q
What fibres connect Frontal and temporal lobes ?
A
UNcinate fasciculus
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
15
Q
How do deeper fibres radiate through the cortex? And what do they converge through?
A
Corona radiata
Internal capsule
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)
17
Q
Prefrontal cortex- what it do?
A
- Adjusting social behaviour
- Personality expression
- Attention
- Planning
- Decision making
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
19
Q
What do temporal lobe lesions do?
A
Leads to agnosia- inability to recognise
Anterograde amnesia
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)
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
22
Q
What is diffusion tensor imaging (DTI)?
A
Based on diffusion of water molecules
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
24
Q
What is TMS?
A
transcranial magnetic stimulation
- Uses electromagnetic induction to stimulate neurones
- assess functional integrity of neural circuits
25
What is transcranial direct current stimulation (tDCS)?
Uses low direct current over the scalp to increase or decrease neuronal firing rates
26
describe what M-waves, F-waves and H reflexes are and what information they can provide.
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.
27
IN an F - wave A large electrical stimulus can cause activation of the motor axons to conduct -------
antidromically
28
Total motor conduction time (TMCT)
time from brain to muscle (MEP latency)
29
Peripheral motor conduction time (PMCT) –
time from spinal cord to muscle along motor axon
30
Peripheral motor conduction time (PMCT) – time from spinal cord to muscle along motor axon can be calculated using the formula:
PMCT = (M latency + F latency-1) /2
31
Central motor conduction time (CMCT) is therefore
TMCT - PMCT
32
Describe the hierarchal organisation of the brain
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
33
Describe the hierarchal organisation of the brain
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
34
Describe the functional segregation of motor control
Motor systems organised in a number of different areas that control different aspect of movemt
35
What are the pyramidal tracts and name them
They pass through the pyramids of the medulla
Corticospinal, corticobulbar
Voluntary movement of body and face
From motor cortex to spinal cord/ cranial nerve
36
What are the extrapyramidal tracts and name them
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
37
Describe the corticospinal tracts , what it passes through and its function
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
38
What does the motor homunculus show?
How much of the brain is devoted to that region
39
What does somatotopic representation show?
From, Where each region of the motor cortex innevrates the muscle
40
What do motor nerves from each of these nuclei do?
Oculomotor nucleus
Trochlear nucleus
Trigeminal motor nucleus
Abducens nucleus
Facial nucleus
Hypoglossal nucleus
Eye
Eye
Jaw
Eye
Face
Tongue
41
Name the extra pyramidal tracts and describe their function
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
42
Upper motor neuron lesion positive signs
Increased abnormal motor function due to loss of inhibitory descending inputs
Spasticity
Hyper reflexia
Clonus
Babinksi sign (extensor plantar responses)
43
Upper motor neuron lesion negative signs
Loss of voluntary motor function (flexors stronger than extensors UL and extensors stronger than flexors in LL)
Paresis
Paralysis
44
Apraxia - description and cause
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
45
Lower motor lesion symptoms
Weakness, Hypotonia, Hyporeflexia, Muscle atrophy, Fasciculations, Fibrillations (EMG)
46
Motor neuron disease is also known as
AMYOTROPHIC LATERAL SCLEROSIS
47
Symptoms of motor neuron disease upper motor signs
Spasticity
Brisk limbs and jaw reflexes
Babinskis sign
Loss of dexterity
Dysarthria
Dysphagia
48
Symptoms of motor neuron disease lower motor symptoms
Weakness, muscle wasting, tongue fasciculations , nasal speech, dysphagia
49
Structure and function of parts of the basal ganglia ( 4)
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
50
Parkinson disease - pathology and symptoms
Degeneration of the dopaminergic neurons that originate in substantial nigra and project to striatum
Bradykinesia
Hypomimic
Akinesia
Rigidity
Tremor at rest
51
Huntington disease- pathophysiology and symptoms
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
52
Ballism- cause and symptom
Stroke affecting subthalamic nucleus
Sudden uncontrollable flinging of extremities
Symptoms contralateral
53
Cerebellum
Location
Separated by cerebrum by
Function
Posterior cranial fossa
tentorium cerebelli
Coordinator and predictor of movement
54
Three cerebellar diseases
Disease of Vestibulocerebellum
Disease of spinocerebellum
Disease of cerebrocerebellum
55
What is the function of the vestibulocerebellum
Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements
56
Lesion of the vestibulocerebellum
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
57
Function of the spinocerebellum
Coordination of speech
Adjustment of muscle tone
Coordination of limb movements
58
Lesion of the spinocerebellum
Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)
59
Functon of the cerebrocerebellum
Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control
60
Lesion of the cerebrocerebellum
Damage affects mainly arms/skilled coordinated movements (tremor) and speech
61
Main signs of cerebellar disease ( appaerant only on movement)
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
62
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?
1. Lower motor neurons of brain stem and spinal cord
2. Extrafusal fibres of skeletal muscle
3. Contraction of muscle
4. Motor neuron pool
63
Motor unit
a single neuron and all the muscle fibres it innervates
64
Slow (S) vs Fast, fatigue resistant ( Type IIa) vs Fast fatiguable ( Type IIb)
Diameter - Increases in diameter
Dendritic tree - Gets larger
Axon - Gets thicker
Conduction velocity - Gets faster
Force generated - Gets larger
65
What are the three different types of motor units characterised by?
amount of tension generated
speed of contraction
fatiguability.
66
Describe the two mechanisms of force generation
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
67
Role of neurotrophic factors
Prevent neuronal death
Promote growth of neurons after injury
68
What are common states that lead to changes in muscle fibre properties. (Plasticity)
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
69
Describe Jendrassik manoeuvre
clenching the teeth, making a fist, or pulling against locked fingers - Makes reflex larger
70
What is seen in hyper- reflexia?
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.
71
What is seen in hypo reflexia?
Below normal or absent reflexes
Associated with lower motor neuron diseases
72
What is a hallmark of pure corticospinal lesion?
Absent abdominal reflex with others present
73
How are headaches classified according to international headache society?
Primary or Secondary Headache
74
Primary vs Secondary Headache syndromes
Primary:
Migraine, Tension-type headache ,Trigeminal autonomic cephalalgias, Cluster headache
Secondary:
Headache is spercipitated by another condition / disorder - local os systemic.
75
How would you further categories primary headaches?
Long lasting >4 hrs
Migraine
Tension type headache
Medication overuse headache
Short lasting < 4 hours
Cluster headache
Trigeminal autonomic cephalalgias
76
Red flag symptoms of headaches
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
Central hypothesis pathology : MIgraine
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
Characteristics of a migraine
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
Features of auras 'migraine'
Expanding 'C's
Elemental visual disturbance
Gradual evolution: 5-30minutes (<60minutes)
Usually before headache
80
MIgraine phases
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
Migraine management:
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
Migraine preventatives
ACE inhibitors
Angiotensin II blockers
Serotonin antagonists
B blockers
Anti convulsants
Anti depressents
Parenteral
83
Characteristics of tension type headache
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
Treatment of tension type headache
Reassurance
Paracetamol
85
Cluster headache characteristics
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
Cluster headache management
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
What is the function of a) vestibular and b) hearing organ?
a) capture low frequency - movement
b) capture high frequency - sound
88
Evolution of the vestibular sensory division
Statocyst --> Utriculus --> Sacculus --> a) Cochlea , Canals
89
Frequency measured in BLANK describes what we call BLANK and is
Hertz
Pitch
Cycles per second, perceived tone.
90
Amplitude measured in BLANK describes what we call BLANK and is
dB
Loudness
Sound pressure, subjective attribute correlated with physical strength.
91
Human range of hearing
Frequency: 20–20,000Hz
Loudness: 0 dB to 120 dB sound pressure level (SPL)
92
Outer ear function
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
Function of the Middle Ear
AMPLIFICATION: The main function of the middle ear is mechanical amplification (can provide an additional 20-30dB)
94
Function of the Inner Ear aka cochlea
TRANSDUCTION- transduce vibration into nervous impulses
CAPTURE SOUND - captures the frequency (or pitch) and intensity (or loudness) of the sound
95
3 compartments of the cochlea
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
Basilar membrane where the structure Organ of Corti ies is arranged
tonotopically,
97
The organ of Corti contains two types of hair cells
Inner hair cells (IHC) and
Outer hair cells (OHC)
98
Tectorial membrane
location and function
above the hair cells and allows hair deflection, which in turn will depolarise the cell.
99
Inner hair cells (IHC) function
carry 95% of the afferent information of the auditory nerve. Their function is the transduction of the sound into nerve impulses
100
Outer hair cells (OHC) function
carry 95% of efferents of the auditory nerve. Their function is modulation of the sensitivity of the response.
101
The hairs of the hair cells are called
stereocilia.
102
Explain transduction of sound in the ear
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
How will louder sounds be affect transduction
Higher amplitudes (louder) of sound will cause greater deflection of stereocilia and K+ channel opening
104
Auditory pathways
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
Types of hearing loss - broad category
Anatomical
106
Anatomical hearing loss
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
Timing of hearing loss
Sudden hearing loss minutes to days
Progressive hearing loss months to years
108
Causes of condusive hearing loss
Outer ear - foreign body, wax
Middle ear - Otitis ( seen by bubbles that suggest fluid in ear) , Otoscleorosis
109
Causes of sensorineural hearing loss
Inner ear - Noise, Presbycusis, Ototoxicity
Nerve - acoustic neuroma (vestibular schwannoma) (unilateral)
110
Two tests for hearing bedside
Weber test - tuning fork over head
Rinne test - tuning fork behind ear
111
WHat is audiometry and what is the difference between conductive and sensironeural
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
Special tests for hearing - Otoacoustic Emissions (OAEs)
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
Treatment for hearing loss
UNderlying cause
Brainstem implants
Hearing aids
Cochlear implants
114
What makes up the vestibular systems?
What is the input, what is the output?
Mechanical sensors (canals and otoliths)
Input: Movement and gravity
Output: Ocular reflex, Postural control
115
How many semicircular cannals are there, describe them ?
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
What are the otolith organs?
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
What is the maculae in relation to the ololith organs?
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
What leads to otolith movement
Linear acceleration and tilt: otolith movement
Utricule: horizontal movement
Saccule: vertical movement
119
What movement causes deflection towards the kinocilium
Head tilt backwards and acceleration
120
What makes up the semicircular canal?
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
Orientation of the canals in the head
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
Hair cell potential in vestibular movement
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
Vestibular nerve and nuclei
Primary afferents end in vestibular nuclei in the brainstem (pons)
124
Vestibular system functions
To detect and inform about head movements
To keep images fixed in the retina during head movements
Balance
125
Vestibular reflexes
Vestibulo-ocular Reflex
(VOR)
Vestibulo Spinal Reflex
(VSR)
126
Describe the Vestibulo-ocular reflex (VOR)
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
Vestibular disorder – how to categorise them
Timing
Laterality
128
What are the main complaints in In acute AND unilateral vestibular disorders?
Main complaints - imbalance, dizziness, vértigo and nausea
129
What are the main complaints In slow AND unilateral or any bilateral loss: vestibular disorders?
Main complaints – imbalance and nausea – NO vertigo
130
Balance disorders: LOCATION
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
Clinical approach for a physician in acute vertigo:
The main diagnosis
The core exam
The main diagnoses
- BPPV
- Vestibular Neuritis
- Vestibular Migraine
- Stroke (cerebellar)
The core exam
EYES
EARS
LEGS
132
Red Flags in vestibular disorders
Headache
Gait problems
Hyper-acute onset
Hearing loss
Prolonged symptoms (>4 days)
133
Balance disorders: Timing (evolution)
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
HINTS exam – clinical exam in acute dizziness
To decide between :
Vestibular Neuritis or Stroke?
*H*ead *I*mpulse Test
Horizontal rotational VOR
*N*ystagmus
Vestibular organ Vs Cerebellar/brainstem nystagmus
*T*est of *S*kew Deviation
Vertical misalignment - usually absent in peripheral pathology
135
What can be done to restore the crystals back in Benign Paroxysmal Positional Vertigo (BPPV)
Epley or Semont.
136
What features can be seen in the MRI of a patient with Dementia?
AB
Neuronal tau
TDP 43
a- synuclein
137
MMSE involves questions in which 6 categories?
What other examination could you do to confirm dementia?
Orientation, Registration, Attention and Calculation, Recall, Language, Copying
ACE III
138
What is the scoring in MMSE
24-30 no cognitive impairment
18 -23 mild cognitive impairment
0- 17 severe cognitive impairment
139
What bloods should you order in testing for dementia?
FBC, CRP, ESR, Thyroid function, Biochemistry and renal function, Glucose, B12 and folate, Clotting, Syphillis serology, HIV, Caeruloplasmin
140
Management of dementia
Acetylcholinesterase inhibitors
Watch and Wait
Treating behavioural/ psychological symptoms
OT/ Social services
Specialist therapies
141
Varients of dementia and features
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
Episodic memory
Memory for particular episodes in life
Dependent on the medial temporal lobes inc hippocampus
143
Spatio - temporal evolution of amyloid and tau according to Thal and Braak
Amyloid - moves from superficial superior to deep inferior ( finally at brain stem)
tau - moves anterior to posterior
144
How can amyloid be detected in vivo?
PET Amyloid
145
Features of Alzheimers disease investigstions
Enlarged ventricles
Narrowed Gyri
Widened sulcus
Atrophy
Hippocampul atrophy
CSF - B amyloid plaque lower, Tau higher than controls
146
Features of FTD investigations
Perisylvian volume decreased - asymmetric
Then genetic test
147
Dementia with Lewy bodies investifations
DAT scan - dopamine presence
In caudate and Putamen in AD but decreased in DLB
148
Inflammation terms define:
Meingitis
Myelitis
Inflammation of meninges- caused by infections, milky white autopsy in subarachnoid on autopsy
Inflammation of the spinal cord
149
What forms the blood brain barrier?
BBB capillaries have extensive tight junctions at the endothelial cell-cell contacts, massively reducing solute and fluid leak across the capillary wall
150
What happens following blood brain barrier dysfunction?
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
Symptoms of encephalitis
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
Causes of encephalitis
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
Treatment of encephalitis
Antivirals e.g. acyclovir
Steroids
Antibiotics/antifungals
Analgesics
Anti-convulsants
Ventilation
154
Cellular pathology of MS
Inflammation
Demyelination
Axonal loss
Neurodegeneration
155
Inflammation in MS caused by?
perivascular immune cell infiltration (CD3 T-cells and CD20 B-cells)
156
Causes of Meningitis
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
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Symptoms of meningitis
sudden fever, severe headache, nausea or vomiting, double vision, drowsiness, sensitivity to bright light, and a stiff neck, rash (not always
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What diagnostic tests can be performed for meningitis? What might be found on these tests?
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.
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What are the three layers of the eye and describe them
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
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Optic nerve description
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
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Macula description
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
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Where is the optic nerve blind spot?
Where the optic nerve meets the retina- there are no light sensitive cells
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Where is the optic nerve blind spot?
Where the optic nerve meets the retina- there are no light sensitive cells
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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?
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
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Peripheral vision:
What part of vision is it involved in?
How is it assessed?
What does loss lead to?
1. Shape, movement, night vision, navigation vision
2. Visual field assessment
3. Unable to navigate in the environment
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What is the structure of the retina and what are their functions?
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
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Refraction - light from one medium to another change
How does the eye accommodate this?
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
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Emmetropia
Ametropia
Descriptions
Emmetropia- adequate correlation between axial length and refractive power, parallel light falls on retina
Ametropia - mismatch between axial length, refractive power
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Types of ametropia
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
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Near response triad description
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
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Presbyopia description and management
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
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Visual Pathway Landmarks
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)
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Lesion at the optic chiasm description
Bitemporal hemianopia
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Lesion posterior to optic chiasm
Right sided lesion- left homonymous hemianopia in both eyes
Left sided lesion- right homonymous hemianopia in both eyes
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Optic chiasm uncrossed vs crossed fibres
Crossed fibres -Originate from nasal retina responsible for temporal visual field
Uncrossed fibres - originating from temporal retina, responsible for nasal visual field
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Homonymous hemianopia with macular sparing
damage to primary visual cortex as area representing macula recieves blood supply from posterior cerebral arteries both sides
Often due to stroke
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Pupillary reflex
where does pupil specific ganglion cells exit?
Describe the pathway
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
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Afferent vs efferent defect seen through pupillary reflex assessment
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
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Swinging torch test (relative damage to afferent)
Both pupils constrict when light shown on undamaged side, but paradoxically both pupils dilate when light shown on damaged side
