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ESA 4 missing > Neuro > Flashcards

Neuro Flashcards

1
Q

action pons vs medulla vs midbrain

A

pons- feeding and sleep

medulla- cvs and resp

midbrain- reflex eye responses

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2
Q

fasiculus vs funinculus vs tract

A

fasciculus- subdivision of a tract supplying a distinct region of the body

funiculus- a segment of white matter containing multiple distinct tracts. bidirectional

tract- white matter pathway connnecting two regions of grey matter

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3
Q

gracile vs cuneate fasiculus

A

gracile- lower
cuneate- upper

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4
Q

3 types of fibres and roles

A

association- same hemisphere
projection- to spinal cord
commisural- to other hemisphere

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5
Q

pre vs post central gyrus

A

pre- motor
post- sensory

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6
Q
A

purple- cingulate gyrus. emotion and memory

red- corpus callosum. fibres connecting two cerebral hemispheres

green- thalamus. sensory relay station projecting to sensory cortex

blue- hypothalamus. homeostasis

yellow- fornix. output pathway from hippocampus

brown- tectum. dorsal part of midbrain involved in involuntary responses to auditory and visual stimuli

cerebellar tonsils- cerebellum that can herniate and compress the medulla

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7
Q
A

yellow- parahuppocampal gyrus. key cortical region for memory encoding.

red- optic chiasm. where visual fibres cross over

green- uncus. part of temporal lobe that can herniate, compressing the midbrain

blue- medullary pyramids. location of descending motor fibres.

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8
Q

abnormal neural tube deficits

A

-craniorachischisis- neural tube remains open,brain and spinal cord don’t form. incompatible with life

-anecephaly- cranial neural tube fails to close. failure of brain to form. may live for a little

-myelocoele- spinal cord does not develop, csf filled cyst. have neurological defects and have meningitis often

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9
Q

which word shows neuro type defecit is present

A

myelo

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10
Q

normal neuro tube defects

A

-myelomeningocoele- CSF filled cyst containing spinal cord. does not transilluminate. neurological defect

-meningocoele- CFS filled cyst. transilluminates. no neurological defect

-spina bifida occulta- lack of posterior vertebral arch, tuft of hair/naevus over deficit. no neurological problems.

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11
Q

why do neural tube defects predispose to hydrocephalus

A
  • cord is tethered at site of defect
  • as spine grows cord cannot move within vertebral canal, causing brainstem to be pulled down through foramen magnum and become occluded
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12
Q

why does the Caudia equine form

A

⇒ A 3 months, the spinal cord is the same length as the vertebral column

⇒ Thereafter, the vertebral column grows faster

⇒ The spinal roots must elongate in order to exit at their intervertebral foramen

⇒ Cauda equina is formed

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13
Q

primary vesicles and what secondary vesicles they form

A

Prosencephalon (Embryonic forebrain)

  • telencephalon and diencephalon
    • ​telencephalon forms cerebral hemispheres
    • diencephalon forms thalamus

Mesencephalon (Embryonic midbrain)

  • Mesencephalon
    • ​Forms midbrain

Rhombencephalon (Embryonic hindbrain)

  • Metencephalon and myelencephalon
    • metencephalon forms pons and cerebellum
    • myelencephalon forms medulla oblongata
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14
Q

what vesicles form which ventricles

A

LV- Telencephalon

3rd- Diencephalon

CA- Mesencephalon

4th- Meten/myelencephalon

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15
Q

where does the MCA supply

A

 Cortical branches emerge from the lateral fissure to supply the lateral
aspect of the cerebral hemisphere (cortex and underlying white matter), including lateral parts of the frontal and parietal lobes as well as the superior temporal lobe

 Deep branches (the lenticulostriate arteries) supply deep grey matter
structures including the lentiform nucleus and caudate as well as the internal capsule

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16
Q

where does the ACA supply

A

 Cortical branches supply the medial aspect of the frontal and parietal
lobes (not the occipital lobe)

 There are also branches to the corpus callosum itself as the ACA loops over the corpus callosum as it sends branches to the adjacent cortex

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17
Q

where does the PCA supply

A

o Supplies occipital lobe, inferior temporal lobe and
thalamus (via thalamoperforator and thalamogeniculate branches)
o Also supplies midbrain en passant

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18
Q

branches of the PCA

A

o Posterior communicating arteries branch from these to
connect with the anterior circulation (internal carotid artery)

• Superior cerebellar artery supplies the superior aspect of the
cerebellum and midbrain en passant

• Pontine arteries supply the pons (including descending
corticospinal fibres)

• Anterior inferior cerebellar artery the supplies the antero-
inferior aspect of the cerebellum and lateral pons en passant

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19
Q

draw circle of willis

A
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20
Q

compare the regions of the body supplied by MCA/ACA

A

mca- upper limb

aca- lowe limb

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21
Q

describe blood supply to the spinal cord

A

anterior 2/3- ASA

posterior 1/3- PSA

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22
Q

describe blood supply to CST, STT and DCML

A

CST/STT- anterior spinal

DCML- posterior spinal

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23
Q

compare PSA and ASA blockage

A

PSA

  • unilateral as the arteries are paired
  • ipsilateral loss of DCML below level

ASA

-midline arteries so effects are bilateral

-loss of STT below level and UMN signs above level due to CST blockage

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24
Q

amacrine

ganglion

horizontal

bipolar

A

amacrine- inhibitory neurons and project their dendrites to the inner plexiform layer to interact with retinal ganglion cells and/or bipolar cells

ganglion- a type of neuron in the retina which receives visual information from photoreceptors via bipolar cells and amacrine cells

horizontal- laterally interconnecting neurons which help integrate and regulate the input from multiple photoreceptor cells

bipolar- cells which exist between photoreceptors in the retina and act indirectly/directly to transmit signals from the photoreceptors to the ganglion cells

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25
Q

left monocular blindness

A

left hand side optic nerve lesion

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26
Q

bitemporal hemianopoa

A

optic chiasm

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27
Q

left hand side homonymous hemianopia

A

right hand side optic tract

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28
Q

left homonymous inferior quadrantinopia

A

right superior optic radiation

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29
Q

describe macula sparing

A

in PCA stroke, the occipital lobe is lost

the MCA supplies the occupital pole and so macula vision is spared

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30
Q

where fo the afferent (CNII) nerve synapse

A

pre tectal area

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31
Q

3 aspects of accomodation reflex

A
  • Convergence (medial rectus)
  • Pupillary Constriction (constrictor pupillae)
  • Convexity of the lens to increase refractive power (ciliary muscle)
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32
Q

compare dcml and stt

A

dcml- lower body medial and upper body lateral

in PSC- lower body medial, upper body lateral

stt- lower body lateral and upper body medial

in PSC- lower body medial, upper body lateral

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33
Q

symptoms brown sequard

A

sensory

  • ipsilateral segmental anaesthesia and dcml loss
  • contralateral stt loss

motor

  • CST lesion: ipsilateral spastic paralysis (due to loss of moderation by the UMN).
  • At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion).
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34
Q

receptive field and visual acuity

A

receptive field- area supplied by a single primary sensory neurone

visual acuity- ability to have two point discirmination

inversely proportionate

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35
Q

where are the cell bodies for primary, secondary and tertiary sensory neurones

A

primary- dorsal root ganglion

secondary- medulla/dorsal horn

tertiary- thalamus

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36
Q

DCML tract

A
  • first order neurone has cell body in DRG. ascends through gracile (lower) or cuneate (upper) fasiculus
  • in medulla synapses with secondary neurone. projected to thalamus
  • at thalamus projects to PSC

lower body = medial

upper body = lateral

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37
Q

STT

A
  • first order neurone has cell body in DRG. synapses with second order neurone in dorsal horn, which decussates at ventral white commisure
  • second order neurone ascends to thalamus, synapses with third order neurone
  • projects to psc

lower body = lateral

upper body = medial

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38
Q

pain modulation

A

C fibres detect pain, AD fibres are inhibitory interneurones activated my mechano receptors.

Additionally, these encephalinergic interneurones can also be activated by
descending inputs from higher centres such as the periaqueductal grey matter or the nucleus raphe magnus

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39
Q

cell bodies LMN vs UMN

A

UMN- primary motor cortex

LMN- ventral spinal cord, motor nuclei in brainstem

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40
Q

describe route the UMN takes to LMN

A

corona radiata

internal capsule

cerebral peduncles (midbrain)

pons

medullary pyramids

decussates

ventral horn

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41
Q

topographical representation in CST compared to motor homunculus

A

in CST- lower limb lateral, upper limb medial

in motor homunculus- lower limb medial, upper limb lateral

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42
Q

what do the ventral and lateral CST supply

A

ventral(15%)- proximal

lateral (85%)- distal

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43
Q

what tract do the UMN supplying face go in

A

corticobulbar

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44
Q
A

MIDBRAIN

1- CNII and EDW nucleus

  1. medial lemniscus
  2. periaquaductal grey matter
  3. cerebral aquaduct
  4. superior colliculus
  5. red nucleus
  6. substandia nigra
  7. cerebral peduncles
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45
Q
A

green- corticospinal tract

pink- thalamic radiations. contaim ascending third order sensory neurones.

blue- corticofugal fibres. from cortex away from brain

yellow- corticobulbar tract

purple- genu

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46
Q

what is the internal capsule

A

bidirectional white matter pathway containing ascending tertiary sensory fibres and descending UMN motor fibres

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47
Q

action of cerebral peduncles, red nucleus and superior colliculus

A

cerebral peduncles- connect cerebral hemispheres to midbrain

red nucleus- motor control

superior colliculus- visual reflexes

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48
Q

effects of direct and indirect pathways normally and under influence of dopamine

A

indirect

- normally inhibitory

  • under dopamine at d2, inhibition is inhibited and so it is stimulatory

direct

  • normally stimulatory
  • under dopamine at d1, excitation is increased.
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49
Q

why is the indirect pathway excitatory under dopamine?

A

the SNc releases dopamine which inhibits the putamen at D2

this inhibits the normal inhibition of the GPe and so increases GPe activity

this increases the GPe inhibition of STN, and so STN activity decreases.

this decreases STN activation of GPI, and so there is less GPi inhibition of the thalamus.

this increases overall cortical activity

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50
Q

why is the direct pathway excitatory under dopamine

A

the SNc excites the putamen at D1

this increases inhibition of the GPi

this then reduces GPi inhibiton of the thalamus

this increases cortical activity

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51
Q

what makes up striatum and lentiform nucleus

A

striatum- caudate nucleus and putamen

lentiform nucleus- putamen and GPi/GPe

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52
Q

where is the lesion parkinsons/huntingtons/hemiballismus

A

parkinsons- the SNc

hemiballismus-STN

huntingtons- loss of inhibitory projections from striatum to GPe

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53
Q

pathophysiology of parkinsons

A

loss of dopaminergic neurones in SNc

less activation of direct pathway via D1

less inhibition of indirect pathway via D2

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54
Q

symptoms parkinsons

A

bradykinesia, rigidity, tremor, hypophonia, micrographia, incontenence, mood changes, dementia

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55
Q

pathophysiology of huntingtons

A
  • loss of inhibiory fibres from striatum to GPe
  • Gpe not inhibited and so more inhibition of STN.

this means less activation of GPi and so less inhibition of thalamus from GPi

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56
Q

symptoms huntingtons

A

chorea, dystonia, loss coordination, cognitive decline

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57
Q

pathophysiology hemiballismus

A

loss of STN.

less activation of GPi.

less thalamic inhibiton from GPi

more cortical activation

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58
Q

why is unilateral basal ganglia damage contralateral, whereas unilateral cerebellar damage is ipsilateral

A

basal ganglia- only the CST decussates

cerebellum- the CST and the rubrospial tract deucssate.

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59
Q

inputs and outputs to cortex

A

inputs- thalamus and cortical areas

outputs-

association fibres eg. arcuate fasiculus

projection fibres eg. UMN

commisural fibres eg. corpus callosum

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60
Q

describe long term potentiaion

A
  • changes in glutamate receptors
  • synaptic strengthening
  • axonal sprouting
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61
Q

describe strorage of short and long term memories

A

short- cortical circuits

long term- cerebellum for non declerative

cerebral cortex for declerative

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62
Q

3 outputs from reticular formation

A

hypothalamus sends histaminergic

thalamus sends glutaminergic

basal forebrain sends cholinergic

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63
Q

EEG trace for different levels of sleep

A

Awake- beta

Drowsy- alpha

I- theta

II/III- sleep spindles (high frequency outbursts) and K+ complexes (intrinsic rate thalamus)

IV- delta

REM- beta

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64
Q

what does EEG measure

A

combined activity of neurones. detects neuronal synchrony

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65
Q

3 sleep disorders

A

narcolepsy, sleep apnoea, insomnia

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66
Q

transtentorial herniation

A

medial parohippocampal gyrus/uncus herniates through tentorial notch.

causes CNIII lesion and disuption in blood supply from the PCA and the superior cerebellar arteries, also motor signs as cerebral peduncle compressed

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67
Q

tonsillar herniation

A

the cerebellar tonsils through foramen magnum

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68
Q

subfalcrine herniation

A

the cingulate gyrus under falx cerebri

  • displaces corpus callosum and lateral ventricle
  • ACA compressed so ischemia of medial frontal and parietal lobes
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69
Q

what is a water shed area

A

– areas that lie at most distal portion of artery territory (border MCA and ACA high risk) – wedge shaped necrosis. Seen after hypotensive episode.

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70
Q

cause stroke

A

Hypertension – 60yrs +, rupture of small intraparenchymal
blood vessels.
Cerebral amyloid angiopathy

Arteriovenous and cavernous malformations

Tumours

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71
Q

effects of hypertension on brain

A
  • Arteriosclerosis (thickened walls) of:
  • Deep penetrating arteries and arterioles:

(1) Basal ganglia and thalamus
(2) White matter
(3) Brainstem

72
Q

what is cerebral amyloid angiopathy, what casues it, effects of it

A
  • Amyloid deposition in the walls of small and medium sized meningeal
    and cortical vessels (congo red stain). causes rigid and inflexible and weakens wall, amd risk of haemorrhage.
  • caused by advancing age, lobar haemorrhages involving the cerebral cortices and tiny
    microhaemorrhages.
73
Q

Arteriovenous malformation

A

– most common, M>F 10-30 yrs age
- subarachnoid vessels to brain / vessels within the brain.

  • wormlike (tangled) vascular channel
74
Q

Cavernous malformations

A

– loose vascular channels, distended, thin
walled.

  • cerebellum and pons
75
Q

Capillary telangiectasia

A

microscopic foci of dilated thin walled
vessels

76
Q

Venous angioma

A

dilated venous channels

77
Q

5 types CNS tumours

A
  • glioma eg. astrocytic
  • parenchymal eg. germ cell
  • meningeal eg. meningioma
  • neuronal eg. ganglion cell
  • poorly differentiated eg. medulloblastoma
78
Q

lymphomas

A

Diffuse, large B cell lymphomas, associated with pt with
EBV

79
Q

Germ cell tumours

A

midline tumours, pineal and suprasellar e.g.
germinoma

80
Q

• Medulloblastoma

A

20% Children, cerebellum, radiosensitive.

81
Q

Meningiomas

A

benign, derived from arachnoid meningothelial cells,
can cause problems if compress important structure / enlarge.

82
Q

bacteria causing meningitis

A

infants- e coli

toddlers- h influenze

young adults- strep pneumoniae

chronic- mycobacterium tuberculosis

83
Q

bacteria causing cerebral abscess and empyema

A

abscess- streptococci/staphylococci

empyema- staphylocicci/anerobic gram negative

84
Q

cause encephalitis

A

Temporal lobe – HZV

Spinal cord MN – Polio

Brainstem - Rabies

85
Q

concequences of prion disease

A

Neuron cell death

Synapse loss

Microvacuolations (spongiform)

Lack of inflammation

86
Q

cause migraine

A

trigeminal neuralgia, sensitised to otherwise ignored stimuli. causes vasodilation of cerebral blood vessels

87
Q

cause and presentation cluster headache

A
  • hypothalamic activation with secondary trigeminal and autonomic involvement
  • sharp stabbing unilateral pain around eye. ipsilateral autonomic features
88
Q

SNOOP

A
  • *S**ystemic
  • *N**eurological
  • *O**nset is new and above 55
  • *O**nset is thunderclap
  • *P**apilloedema, postiona, exercise
89
Q

cause and presenation giant cell arteitis

A

vasculitis in large and medium sized arteries, usually temporal

sudden onset jaw claudication with headache and visual disturbances. can cause visual loss due to disruption to CNII blood supply

90
Q

cause and presentation trigeminal neuralgia

A

compression of CNV by loop of blood vessel

pain in 1+ CNV division, stabbing unilateral facial pain that is triggered by chewing or similar activities or by touching affected areas on the face

91
Q

reversible causes of dementia

A

hypothyroidiam, hypercalcaemia, B12 deficiency

92
Q

changes to brain in dementia

A

global cortical atrophy, sulcal widening, ventricular dilation

93
Q

describe beta amyloid plaques

A

amyloid precursor broken down by beta secretase, forms insoluble plaques

these cause

  • amyloid angiopathy that weakens blood vessels
  • inflammation causing neuronal death
  • reduction in neuronal transmission
94
Q

patho lewy body dementia

A

alpha synuclein protein incorrectly broken down and forms lewy body deposits in substantia nigra and cortex.

95
Q

specific lewy body symptoms

A

hallucinations, REM sleep disturbance, falls due to parkinsonism

96
Q

specific symptoms frontotemporal dementia

A

behaviour disinhibition, innapropriate social behaviour, loss motivation, broca’s aphasia

97
Q

treatment dementia

A

acetylcholinesterase inhibitors- donepezil

NMDA antagonists- memantine

98
Q

cause delerium

A

B12 deficiency, stroke, infections, withdrawal

99
Q

ACA

A

incontenence

CL lower body motor and sensory loss

dysarthia

apraxia

alien hand syndrome

100
Q

MCA stroke

A

proximal

  • hemiparesis CL
  • CL upper body sensory loss
  • global aphasia
  • CL homonymous hemianopia

Distal

S - CL motor loss and expressive dysphasia

I- Cl sensory loss, Cl HH, and receptive dysphasia

Lacunar

pure sensory/motor or sensorimotor

101
Q

PCA stroke

A

Cl sensory loss, HH w macula sparing

102
Q

brainstem stroke

A

CL motor and IL cranial nerves

103
Q

Cerebellar

A

IL horners and cerbellar signs

CL sensory

104
Q

basillar

A

distal- hallucinations, somlomence, CNIII

proximal- locked im

105
Q

PACS/TACS vs POCS

A

PACS/TACS

  • visulospatial, HH, CL motor/sensory, aphasia

POCS

  • cranial nerves, bilateral motor/sensory, conugate eye movemen, cerebeller signs, HH w/ macula sparing
106
Q

lumbar puncture in subarachnoid haemorrhage

A

increased opening pressure

xanthochromia

increased protein

high red cell

WCC and glucose normal

107
Q

ACA vs PCA specific effects on other structures

A

ACA- optic chiasm, pituitary, frontal

PCA- CNIII palsy

108
Q

xray raised ICP

A

midline shift, ventricular effacement, loss grey/white matter differentiation

109
Q

describe limis to cerebral autoregulation

A

below 50mmHg cannot vasodilate more, above 150mmHg cannot vasoconstrict more

110
Q

equation CPP

A

CPP = MAP- ICP

111
Q

cushings triad

A

widened pulse pressure, bradycardia, and irregular respirations

poor prognostic factor

112
Q

areas involved in limbic system

A

amygdala, septal area, pre frontal cortex, hipppocampal area, cingulate gyrus

113
Q

role hippocampus limbic syste

A

o Receives inputs from many parts of the cortex and processes their emotional content

o projects to the thalamus and also to the hypothalamus (causing autonomic features of emotional responses, since the hypothalamus send projections down through the cord to autonomic preganglionic neurones – the hypothalamospinal tract. This will lead to sympathetic nervous system activation, as well as release of adrenaline from the adrenal medulla – the acute stress response)
o Role in memory – already discussed

114
Q

role amygdala

A

o Receives many inputs from the sensory system

o Major outputs to cortex and hypothalamus o Like the hippocampus, involved in behavioural and autonomic emotional responses

115
Q

role prefrontal cortex

A

o Modulation of emotional responses (e.g. consciously suppressing features of anxiety)
o ‘Perception’ of emotion

116
Q

describe HPA axis

A

hypothalamuc releases CRH

pituitary releases ACTH

adrenal medulla releases noradrenaline, adrenal cortex releases cortisol

117
Q

treatment PTSD

A

treatment
 Biological
• SSRIs • Maybe short term benzodiazepines
 Psychological
• CBT • Eye movement desensitization reprocessing therapy

118
Q

pathophysiology PTSD

A

• Evidence of amygdala hyperactivity causing exaggerated
behavioural responses

• However, low levels of cortisol!

119
Q

patho OCD

A
  • basal ganglia re entry due to direct pathway overactivity
  • reduced SSRIs
  • autoimmune- PANDAS (post strep)
120
Q

treatment OCD

A

 Biological
• SSRIs +/- antipsychotics

• Deep brain stimulation?

 Psychological

• CBT and variety of other interventions

121
Q

symptoms anxiety

A

smptoms – primarily attributable to sympathetic activation
 Palpitations
 Sweating
 Trembling or shaking
 Dry mouth
 Difficulty breathing
 Chest pain or discomfort
 Nausea or abdominal distress (e.g. butterflies in stomach)
 Feeling dizzy, unsteady, faint or light-headed

122
Q

patho and treatment anxiety

A
  • low GABA and serotonin
  • short term benzodiazapines, SSRIs
123
Q

actions cortisol

A

supress immune, allergic and inflammatory responses

increase energy metabolite

124
Q

general adaptation syndrome

A

o Stage 1: The alarm reaction
 Release of adrenaline and cortisol as well as sympathetic activation (described above)

o Stage 2: Resistance (effect of adrenaline starts to wear off)  Chronic stress response, prolonged release of cortisol

o Stage 3: Exhaustion (when you cannot escape an ongoing stressor)  Chronic side effects of prolonged cortisol secretion start to occur

125
Q

mesolimbic pathway

A

from ventral tegmental area to the limbic structures and nucleus acumbens

126
Q

mesocortical pathway

A

ventral tegmental area to frontal cortex and cingulate cortex

127
Q

brain changes schizophrenia

A

enlarged ventricles

reduced grey matter

decreased temporal lobe volume

reduced limbic

128
Q

neuropathology of schizophrenia

A

decreased presynaptic markers, oligodendroglia, thalamic neurones

129
Q

typical vs atypical antipsychotics

A

typical- block D2 receptors. act on mesolimbic and mesocortical

atypical- block 5HT3, dissociate rapidly from D2. weight gain

130
Q

nigrstriatal pathway

A

from substantia nigra pars compacta to the striatum

131
Q

symptoms and cause catotonia

A

stupor, excitement, rigidity, wavy flexibility

caused by less GABA so less inhibition

132
Q

tuberoinfundibular pathway

A

from arcuate and preventricular nuclei to infundibular region of hypothalamus

133
Q

which is raised in schizophrenia

A

more mesolimibic, less mesocortical

134
Q

structural changes schizophrenia

A

enlarged ventricles, decreased grey matter, decreased temporal lobe volume

135
Q

where is serotonin produced

A

raphe nuclei

136
Q

where is NA produced

A

locus corleus

137
Q

treatment of

  • acute mania
  • acute bipolar depression
A

mania: antipsychotic plus mood stabilsier eg. lithium
depression: antidepressant with mood stabiliser cover

138
Q

action astrocytes

A

• Provide structural support

• Nutritional support
o Convert glucose to lactate which they transfer to
neurones
• Reuptake of neurotransmitters

• Maintain ion concentrations in extracellular fluid
o Particularly potassium, which is released in large
quantities in highly active areas of brain
• Contribute to the blood brain barrier
o Induce expression of tight junctions between brain

139
Q

what is immune privilege

A

There is constant surveillance of the CNS by immune cells, however
their activity is tightly regulated

▪ This tight regulation is essential since a strong inflammatory response
in the brain would leads to swelling and hence raised intracranial
pressure (bad)

140
Q

3 types of NT and example

A

amino acids- GABA (GABAA/GABAB), glutamate (AMPA, NMDA), glyceine

biogenic amines- ACh, NA, DA, 5HT, H

Peptides- dynorphin, encephalin

141
Q

where is serotonin and NA formed

A

5HT- raphe nuclei

NA- locus corleus

142
Q

which disease causes by loss of ACh

A

Alzhimers

143
Q

which disease caused by loss of DA

A

parkinsons

144
Q

describe long term potentiation

A

• If the synapse is activated strongly, and a lot of glutamate is
released then additional AMPA receptors are inserted into the
postsynaptic membrane
• This is mediated by the entry of Ca through NMDA receptors

• Extra AMPA receptors means that the synapse will transmit
more readily (i.e. it ‘stronger’
• This is the process of long term potentiation (LTP) which is the
molecular basis for learning and memory

145
Q
A

light green- lateral corticospinal tract

dark green- ventral corticospinal tract

purple- DCML

pink- STT- pain and temperature

peach- ventral STT- light touch

146
Q

which lobe is hippocampus in

A

temporal

147
Q

role cerebral peduncles and another name for them

A

connect cerebral hemispheres

  • crus cerebri
148
Q

Amaurosis fugax effects and cause

A

Amaurosis fugax is a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina

central retinal artery occlusion

149
Q

1st rank symptoms of schizophrenia

A

auditory hallucinations:

thought withdrawal, insertion and interruption.

thought broadcasting.

somatic hallucinations.

delusional perception.

feelings or actions experienced as made or influenced by external agents.

150
Q

what does raphe nuclei form

A

serotonin

151
Q

can thalamus damage affect movement

A

yes

152
Q

what things are required for balance

A
  • vision
  • proprioception
  • vestibular system

2/3 of these

153
Q

what is internuclear opthalmoplegia?

A

ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron between two nuclei of cranial nerves (CN) VI and CN III

due to medial longitudinal fasiculus damage

154
Q

what do photoreceptors synapse with

A

bipolar cells

155
Q

how to determine if lesion is optic tract vs PVC

A

optic tract will show no macula sparing, PVC will

156
Q

which pathway is responsible for loss of conjugate vision

A

medial longitudinal fasiculus

connects CN III, IV and VI

157
Q

how can blockage of CA affect vision

A

compress third nerve nuclei which contains EDW and CNIII

158
Q

are LMN affected by sharp cord transection between c3 c4

A

no, as they only exit at the level, not inbetween

159
Q

where do spinal nerves exit?

A

cervical- above. eg. if c2/c3 cord transected, c3 would be affected

thoracic- exit below. if t2/t3 transected, t2 would be affected

160
Q

action medial longitudinal fasiculus

A
  • allows for conjugate movement
  • inhibition of contralateral extraocular muscles
161
Q

where does spinal cord terminate

A

L1/L2

162
Q

how to increase reflexes

A

jendrassik manouver

163
Q

where is SNc located

A

midbrain

164
Q

what does rhombergs test show

A

sensory ataxia

165
Q

patho sleep apnoe

A

not enough light reaching the brain

166
Q

treatment sleep apnoea

A

postivie pressure mask, lose weight

167
Q

role red nucleus

A

motor control

168
Q

where do thalamoperforator branch from

A

PCA

169
Q

where are cell bodies and dendrites located

A

grey matter

170
Q

raphe nucleus forms…

A

serotonin/ 5HT3

raphe = 5HT3

171
Q

anterior central sulcus

A

primary motor cortex

172
Q

superior colliculus is in the …

A

midbrain

173
Q

cerebellar artery also supplies the …

A

midbrain

174
Q

internuclear ophalmoplegia is caused by damage to …

A

medial longitudinal fasiculus

175
Q

tetorium cerebelli is at the level of the

A

midbrain

176
Q

short term consequences of subarachnoid haemorrhage

A
  • microthrombi occlude small distal arteries
  • vasoconstriction from CSF irritant
  • cerebral oedema
  • sympathetic activation causing myocardial necrosis
177
Q

long term consequence of subarachnoid haemorrhage

A

early rebreeding, acute hydrocephalus, global cerebral ischemia

ESA 4 missing (5 decks)

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