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Medicine year 2 semester 2 > Case 21- Psychoses and Anatomy > Flashcards

Case 21- Psychoses and Anatomy Flashcards

1
Q

The brain changes in Schizophrenia

A

Individuals with Schizophrenia have a smaller hippocampus, increased activity in this region

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2
Q

Temporal lobe and hormones

A
  • Glutamatergic neurones feed into the hippocampus
  • The GABAeric interneurones inhibit the pyramidal excitatory hippocampal neurones
  • This creates highly regulated and controlled output to the ventral tegmental area (VTA)
  • The VTA is the origin of mesolimbic and mesocortical pathways
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3
Q

Temporal lobe in Schizophrenia

A
  • The GABAergic neurones become damaged which is potentially the cause of the reduction in the size of the hippocampus
  • This damage means that there is reduced inhibition and control in the area which may increase activity.
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4
Q

Physiology of the reward pathway

A
  • Reward- involves activation of the VTA neurones and inhibition of activity of the n.accumbens output neurones
  • VTA-accumbens dopamine neurones- driven by glutamate (AMPA-R, NMDA-R) and acetylcholine (nicotinic ACH-R) its inhibited by GABA (GABA-A, GABA-B)
  • D2 dopamine receptors are inhibitory, activating these receptors decrease the firing in the accumbens output
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5
Q

Other pathways in the temporal lobe- NMDA hypofunction

A

Glutamatergic neurons and GABAergic neurons are involved in controlling the level of activity of neuronal pathways in schizophrenia:
• NMDA receptor hypofunction- may reduce mesocortical dopamaminergic activity, decrease in dopamine release in the prefrontal cortex causes negative symptoms
• NMDA may affect GABAergic interneurons- alters cortical processing, cognitive impairment
• NMDA hypofunction removes GABA inhibition of VTA- enhances dopamine release in mesolimbic area, causes positive symptoms

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6
Q

Dopamine

A

A biogenic amine neurotransmitter. Plays an important role in coordinating muscle movement. Involved in motivation, reward and reinforcement learning
Synthesis= Tyrosine -> Dihydroxyphenylalanine (DOPA) -> Dopamine
The 4 dopamine pathways- Mesocortical, Mesolimbic, Nigrostriatal, Tuberoinfundibular

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7
Q

Dopamine receptors and release

A

Dopamine has 5 receptors D1, D2, D3, D4 and D5 all of which are G-protein coupled receptors. Can have an intracellular or excitatory effect depending on the receptor. Its reabsorbed from the synaptic cleft via the dopamine active transporter (DAT) and recycled back into vesicles. Its broken down by catechol-O-methyltransferase and monoamine oxidase

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8
Q

Positive symptoms of schizophrenia

A

1) Agitation
2) Conceptual disorganisation
3) Delusions
4) Grandiosity
5) Hallucinations
6) Hostility, Paranoia, Suspician

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9
Q

Negative symptoms of schizophrenia

A

1) Apathy
2) Absent, blunted or incongurous emotional response
3) Reduction in speech
4) Social withdrawal
5) Impaired attention
6) Anhedonia
7) Sexual problems
8) Lethargy

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10
Q

Dopamine Mesocortical pathway

A

From the ventral tegmental area (VTA) to the Mesocortical area (Prefrontal cortex). The purpose of this pathway is cognition and mood/emotions. In Schitzophrenia underactivity of dopamine in this area results in negative symptoms like low energy and apathy

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11
Q

Dopamine Mesolimbic pathway

A

From the ventral tegmental area (VTA) to the mesolimbic area. Which is the ventral striatum of the basal ganglia in the forebrain. The purpose of this area is reward, addiction and sensory processing. In Schizophrenia overactivity/excess of dopamine in this region causes positive symptoms like hallucinations, delusions and disordered thoughts

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12
Q

Dopamine Nigrostriatal pathway

A

From the substantia nigra to the striatum. Its part of the extrapyramidal motor system and is involved in the initiation and control of movement. Parkinsons disease is caused by defects in the pathway when a loss of neurones in the substantia nigra causes a deficit of dopamine.

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13
Q

Dopamine Tuberoinfundibular pathway

A

Projects from the infundibular nucleus i.e. the arcuate nucleus in the hypothalamus to the anterior pituitary. Dopamine acts as prolactin release inhibiting factor (PRIF) which causes tonic inhibition of lactation by binding to dopamine D2 receptors. Some of the antipsychotic drugs exert their effects by binding to the dopamine D2 receptors which will result in an increase of prolactin which in turn can lead to galactorrhoea and gynaecomastia.

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14
Q

Noradrenaline/norepinephrine

A

A biogenic amine neurotransmitter. It projects predominantly to the forebrain region. Involved in sleep, wakefulness, arousal, attention as well as feeding behaviour
Synthesis= Tyrosine -> Dihydroxyphenylalanine (DOPA) -> Dopamine -> Norepinephrine
Pathways- goes to large areas of the brain, the Cerebellum, Cerebral cortex, Thalamus, Limbic system.
Purpose- arousal/wakefulness, attention, feeding behaviour

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15
Q

Noradrenaline/Norepinephrine- release, receptor binding, reabsorption

A

Release and receptor binding= It binds to ∝ and B adrenergic G-protein coupled receptors. It has an excitatory effect.
Reabsorption= Noradrenaline is reabsorbed via the norepinephrine transporter (NET). It is broken down by catechol-O-methyltransferase and monoamine oxidase.

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16
Q

Serotonine/5-hydroxytryptamine

A

It’s a biogenic amine neurotransmitter. Its primarily produced in neurons within the raphe nuclei which are found in the pons and brainstem. Its likely that every neurone in the brain receives serotonergic innervation. Regulates sleep and wakefulness. Interacts with the dopamine pathway.
Synthesis= Tryptophan -> 5-hydroxytryptophan -> 5-hydroxytryptamine

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17
Q

Serotonin- release, receptor binding and reabsorption

A

Release and receptor binding- It binds to G-protein coupled and ionotropic receptors There are 15 types of serotonin receptors and can have both inhibitory and excitatory effects.
Reabsorption= Serotonin is reabsorbed from the synaptic cleft by the 5-hydroxytryptamine transporter (5-HTT / SERT). Many antidepressant drugs are selective serotonin reuptake inhibitors. It is broken down by monoamine oxidase.

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18
Q

Serotonin- pathways, functions and clinical relevance

A

Pathways- starts at the raphe nuclei in the brainstem. There are connection to large areas of the brain Cerebellum, Cerebral cortex, Striatum (caudate putamen) and the Hippocampus.
Functions- controls arousal, sleep/wake cycle, mood behaviour, appetitive.
Clinical relevance- a serotonin deficit is implicated in the development of depression and anxiety.

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19
Q

Acetylcholine

A

Its an amino acid neurotransmitter. Is a neurotransmitter in the CNS as well as the skeletal neuromuscular junction. Acetylcholinesterase breaks down acetylcholine into acetate and choline. It has both excitatory and inhibitory effects. Choline is reabsorbed via the choline transporter (ChT)

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20
Q

Acetylcholine- two pathways

A
  • Basal forebrain nuclei- large parts of the cortex, Thalamus, Amygdala, Hippocampus
  • Dorsolateral pontine/tegmental region- Cerebellum, Spinal cord, Thalamus, Hypothalamus, Amygdala, Hippocampus
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21
Q

Glutamate

A

Its an amino acid neurotransmitter. It’s the main excitatory neurotransmitter in the CNS, about half of all brain synapses release glutamate. Excessive release of glutamate during trauma can cause excitotoxic brain damage. Doesn’t cross the blood brain barrier meaning its synthesised in the neurons from local precursors. The major receptors targeted by glutamate are the AMPA, NMDA and Kainate receptors.

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22
Q

Glutamate- synthesis, release, receptor binding, reabsorption

A

Synthesis= Glutamine -> Glutamate
Release and receptor binding- It binds to ionotropic AMPA, N-Methyl-D-aspartate (NMDA) and kainate G-protein coupled receptors. It is the main excitatory neurotransmitter.
It is reabsorbed by the excitatory amino acid transporters.

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23
Q

Glutamate pathways

A

Used throughout the CNS, however, there are some major pathways:
• Cortex to nucleus accumbens
• Cortex to basal ganglia
• Cortex to brainstem nuclei (Raphe, VTA, Locus ceruleus etc)
• Pathways within the cortex

24
Q

GABA

A

An amino acid neurotransmitter. A major inhibitory neurotransmitter about a third of all synapses in the brain release GABA. Its predominantly present in local interneurons
Synthesis= Glucose -> Glutamate -> GABA
Release and receptor binding= It binds to ionotropic GABAA/C and metabotropic GABAB receptors. It is the main inhibitory neurotransmitter. It is reabsorbed via the GABA transporter (GAT).

25
Q

GABA pathways

A
  • Local interneuron circuits
  • Cerebellum (Purkinje cells)
  • Medium spiny neurons of the striatum
26
Q

Dopamine theory of schizophrenia

A

It is thought that overactivity/excess of dopamine in the mesolimbic pathway generate positive symptoms and hypoactivity of dopamine in the mesocortical area leads to the negative symptoms of schitzophrenia.

27
Q

Evaluate the dopamine theory of schizophrenia

A
  • Drugs like amphetamines, cocaine, L-dopa, and bromocriptine increase dopamine-related activity in the brain and can induce psychotic symptoms.
  • Our main pharmacological approach in schizophrenia is the use of dopamine antagonists.
  • With further research into this field, it is now believed that the picture is more complicated due to the interactions of multiple neurotransmitter pathways in the brain.
  • Glutamate dysfunction and serotonin overactivity are also thought to be involved.
  • The affinity of antipsychotics for dopamine D2 receptors correlates with therapeutic efficacy
28
Q

Muscles of the eye- Superior rectus

A 
CNIII (Oculomotor), Elevation, intorsion, adduction (up and in). 
Abducted eye (lateral)- elevation
Adducted eye (medial)- Intorsions
29
Q

Muscles of the eye- Superior oblique

A 
CNIV (Trochlear), Intorsion, depression, abduction (down and out). Attached by the Trochlea which makes it work like a pulley system, sits along the medial wall and then attaches to the superior surface of the sclera. 
Abducted eye (lateral)- Intorsion
Adducted eye (medial)- Depression
30
Q

Muscles of the eye- Medial rectus

A

CNIII (Oculomotor), Adduction. Extends from the common tendinous ring and attaches to the Sclera
Abduction/Adduction- Adduction

31
Q

Muscles of the eye- Lateral rectus

A

CNVI (Abducent), Abduction. Extends from the common tendinous ring and attaches to the lateral surface of the Sclera.
Abducted/Adducted eye- Abduction

32
Q

Muscles of the eye- inferior rectus

A 
CNIII (Oculomotor), Depression, extorsion, adduction (down and in). 
Abducted eye (lateral)- depression
Adducted eye (medial)- extorsion
33
Q

Muscles of the eye- inferior oblique

A 
CNIII (Oculomotor), Extorsion, elevation, abduction (up and out). Goes from the medial surface of the orbit and attaches to the inferior surface of the sclera. 
Abducted eye (lateral)- Extorsion
Adducted eye (medial)- elevation
34
Q

How do we look towards the right and left

A

When we look towards the right, the medial rectus of the left eye and the lateral rectus of the right eye contract together.
When we look towards the left, the medial rectus of the right eye and the lateral rectus of the left eye contracts together

35
Q

Medial and lateral rectus- testing of the EOM

A
  • Medial and lateral rectus muscles operate on the X axis
  • They adduct and abduct the eye
  • The actions of the muscles are tested by simply asking the patient to adduct (medial) or abduct (lateral) their eyes
  • Their movements correspond to the actions we ask our patients to do during clinical testing
36
Q

Superior rectus and inferior oblique- testing of the EOM

A
  • Both superior rectus and inferior oblique act to elevate the eye
  • So by asking the patient to look upwards you cannot separate the actions of these muscles and identify the problem. Instead you need to
  • Tests superior rectus- abduct (lateral) and then elevate the eye
  • Tests inferior oblique- adduct (medial) and then elevate the eye
37
Q

Superior rectus- how clinical test works (abduction and elevation)

A
  • Contraction causes the eye to move up and in
  • When the eye is abducted the axis of the superior rectus lines up with that of the eyeball
  • Contraction causes elevation of the eye
38
Q

Inferior oblique- how clinical testing works (adduction and then elevation)

A
  • Contraction causes the eye to move up and out
  • When the eye is adducted the axis of the inferior oblique lines up with that of the eyeball
  • Contraction causes elevation of the eye
39
Q

Testing the superior oblique and inferior rectus muscle

A
  • Both the superior oblique and the inferior rectus act to depress the eye
  • So, by asking the patient to look downwards you cant separate the actions of these muscles and identify a problem. Instead you need to ask:
  • Test inferior rectus- abduct and then depress the eye
  • Tests superior oblique- adduct and then depress the eye
40
Q

Superior oblique- how clinical testing works (adduction and then depression)

A
  • Contraction causes the eye to move down and out
  • When the eye is adducted the axis of the superior oblique lines up with that of the eyeball
  • Contraction causes depression of the eye
41
Q

Inferior rectus- how clinical testing works (abduction and then depression)

A
  • Contraction causes the eye to move down and in
  • When the eye abducted the axis of the inferior rectus lines up with that of the eyeball
  • Contraction causes depression of the eye
42
Q

Arterial supply to the eye

A

Ophthalmic artery (a branch of the internal carotid artery). It enters the orbit with the optic nerve via the optic canal. The branches of the ophthalmic artery can be divided by function, either ocular or orbital

43
Q

Blood supply to the ocular (eyeball)

A
  • Central retinal artery- breaches the optic sheath, branches into 4 to supply the quadrants of the inner retina, the quadrants are the superior temporal, inferior temporal, superior nasal and inferior nasal. Forms a network in the nerve fibre layer. Travels to the eye in the centre of the optic nerve, enters via the optic disk.
  • Posterior ciliary (long and short)
  • Muscular (supplies the EOM and gives off the anterior ciliary)
44
Q

Orbital blood supply

A
  • Lacrimal
  • Posterior ethmoidal
  • Anterior ethmoidal
  • Supraorbital
  • Median palpebral
  • Supratrochlear
  • Dorsal nasal
45
Q

Pathology- central retinal artery occlusion

A
  • Risk factors- all CV risk factors
  • Symptoms- unilateral, painless, lasting visual loss
  • On examination- pale retina, cherry red spot of macula, visual field loss, loss of visual acuity
46
Q

Ciliary arteries- Ocular supply

A
  • Short posterior ciliary- posterior choroid and anastomose around the optic disc to form the circle of Zen
  • Long posterior ciliary artery- anterior choroid, ciliary body and iris
  • Anterior ciliary artery- sclera and rectus muscles. Pierce the sclera near the limbus and form the circular arterious major near the limbus. Anastomose with the long posterior ciliary artery
47
Q

Venous drainage of the eye

A
  • Superior ophthalmic vein- exits via the superior orbital fissure and enter the cavernous sinus
  • Central retinal vein- run through the optic nerve and drain into the superior ophthalmic vein or the cavernous sinus
  • Vorticose veins- drain the vascular layer of the eyeball
  • Inferior ophthalmic vein- can enter into the superior ophthalmic vein or exit the superior orbital fissure on its own or join the pterygoid plexus of veins exiting via the inferior orbital fissure
  • Drainage via the cavernous sinus offers a route for the intracranial spread of infection
48
Q

CN II- Optic nerve

A

Enters the orbit via the optic canal. Passes within the common tendinous ring. Involved in the special senses- vision

49
Q

CN III- Occulomotor nerve

A

• Superior and inferior branches
• They enter the orbit via the superior orbital fissure within the common tendinous ring
• CN III send a parasympathetic root to the ciliary ganglion
• The superior branch supplies the Levator palpebrae superioris and the Superior rectus. Other branches go on to the medial rectus and inferior rectus.
The postganglionic parasympathetic fibres supply:
• Sphincter pupillae- reduces the pupil size
• Ciliary muscle- accommodation of the lens, when the muscle contracts the zonules fibres relax and the lens becomes fatter and an increased refractive power of the lens for near vision

50
Q

CN IV- Trochlea nerve

A
  • Enters the orbit via the superior orbital fissure
  • Runs outside the common tendinous ring
  • Supplies the superior oblique muscle
51
Q

CN V- Trigeminal nerve

A
  • The ophthalmic division or V1 gives sensory innervation to the cornea, this is tested during the corneal reflex. CNVII provides the motor function in the reflex. Sends signals to the trigeminal sensory nucleus and communicates with the facial motor nucleus. Send signals via the facial nerve to the Obicularis oculi muscle which closes the eye
  • There are 3 main branches of this nerve which enter the orbit via the superior orbital fissure- Nasociliary (also passes through the common tendinous ring), Frontal (superior), Lacrimal (goes to the lacrimal gland).
52
Q

CN VI (Abducens)

A

Enters the orbit via the superior orbital fissure, runs within the common tendinous ring. Supplies the lateral rectus muscle

53
Q

Sympathetic nerve supply to the eye

A

Supplies the Superior tarsal muscle (within the eyelid) and the Dilator pupillae making the pupils bigger

54
Q

CNIII- Oculomotor nerve palsy

A
  • Full ptosis- levator palpebrae superioris is inactive
  • Dilation of the pupil- the tone of the sphincter pupillae is reduced due to loss of parasympathetic supply from cranial nerve III.
  • Downward and outwards movement of the eye- only the superior oblique and the lateral rectus can function
55
Q

CN IV- Trochlea nerve palsy

A
  • Elevation and extorsion of the eye- loss of function of superior oblique which intorts and depresses the eye
  • Patients put their chin down and head tilted towards the normal side to compensate for these movements
56
Q

CN VI- Abducens nerve palsy

A

The eye is unable to abduct due to loss of function of the lateral rectus

57
Q

Interruption of sympathetic supply to the eye

A

Can produce Horner’s syndrome:

  1. Partial ptosis- drooping eyelid
  2. Miosis- small pupil
  3. Anhidrosis- reduction in sweat production

Medicine year 2 semester 2 (47 decks)

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