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EOP 1 > Neuro - Phase 1 > Flashcards

Neuro - Phase 1 Flashcards

1
Q

What is the pathophysiology of seizures?

A

Seizures are typically a result of a disruption of the normal balance of inhibitory/excitatory neurotransmission of the brain
• glutamate – excitatory, inward Na+ and Ca2+
• GABA – inhibitory, inward Cl- and outward K+
- variation in this balance can lead to loss of inhibitory GABA mechanisms resulting in disinhibition and a state of neuron hyperexcitability

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2
Q

What are some causes of seizures?

A

wide range of potential causes: VITAMIN D

Vascular – Stroke, embolism

Infection

Trauma

Autoimmune - SLE

Metabolic – hypoglycaemia, Electrolyte imbalances

Idiopathic

Neoplastic

Drugs/medications/EtOH

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3
Q

What are the four major mechanisms of action for seizure drugs?

A
  1. blocking VGSCs to reduce AP transmission – phenytoin, carbamazepine, valproate, lamotrigine
  2. blocking VGCCs to reduce neurotransmitter release – ethosuximide, gabapentin/pregabalin
  3. increasing GABAergic activity – barbiturates, benzodiazepines, valproate, vigabatrin, tiagabine
  4. reducing glutamatergic activity – topiramate, lamotrigine

NB. VGSCs & VGCCs -> voltage gated sodium & calcium channels

Arch:

According to ninja nerd pic:

  1. VGSC blockers - reduce AP transmission
  • Valproate
  • Carbamezapine
  • Phenytoin
  • Lamotrigine

2. VGCC blockers - reduce neurotranmitter release

  • Gabapentin/pregabalin
  • Ethosuximide

3. SV2A blockers - prevent Ca2+ from binding to receptor and prevent neurotranmitter release

  • Levetiracetam (Brand name Keppra)

4. GABA Receptor Agonists - increase GABA activity

  • Benzodiazepines e.g. diazepam, midazolam
  • Propofol
  • Barbiturates

5. NDMA/AMPA inhibitors - Inhibit glumate stimulation on post synaptic cleft

  • Ketamine

6. GABA transaminase inhibitors - prevent the breakdown of GABA

  • Valproate
  • Vigabatrine
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4
Q

First line seizure treatment is generally comprised of what drug?

A
  • valproate is most common 1st line drug except in women of childbearing age due to teratogenic effect -> carbamazepine is often used instead
  • ethosuximide for absence seizures (ie. petit mal seizures- staring into space for a number of seconds)
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5
Q

What are the definitions of:

  • *seizure =**
  • *epilepsy =**
  • *status epilepticus =**
A

seizure = sudden change in brain activity caused by electrical hypersynchronisation of neurons
epilepsy = disorder of recurrent unprovoked seizures
status epilepticus = continuous or recurring seizures that may result in brain injury

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6
Q

What are partial/focal seizures and what are the two subdivisions?

A

• partial/focal – affect a single area of the brain, can have secondary generalisation
o simple partial: consciousness intact
o complex partial: loss of consciousness

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7
Q

What are general seizures and what are the five subdivisions?

A

Generalized seizures happen when abnormal electric activity is set off in both halves (hemispheres) of the brain

o absence: sudden lapse in awareness
o myoclonic: sudden single jerks of muscles
o tonic-clonic: alternating stiffening and jerking
o tonic: stiffening
o atonic: “drop” seizures

NB: Tonic –> stiffening (think toning the body) and clonic is jerking (think clonus of the knee in MSK exam)

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8
Q

Types of brain bleeds

A
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9
Q

What are the four dopaminergic pathways?

A

mesolimbic – VTA to nucleus accumbens (reward)
mesocortical – VTA to prefrontal cortex (cognition)
nigrostriatal – SNpc to striatum (motor loops)
tuberoinfundibular – hypothalamus to pituitary (inhibits prolactin)

NB. VTA is ventral tegmental area, SNpc is substantia nigra pars compacta

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10
Q

What are the four categories of brain development milestones?

A
  • gross motor
  • fine motor
  • language development
  • social development
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11
Q

What is the physiological process of hearing within the inner ear from the ossicles to the stereocilia?

A

the auditory ossicles transmit sound waves into mechanical vibration, which is directed onto the oval window, this causes perilymph to move through the cochlea

  • results in movement of basilar membrane which contains hair cells in the organ of Corti
  • bending of stereocilia on hair cells causes depolarisation and AP generation
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12
Q

What is the neurological pathway of hearing from the stereocilia hair cells to the primary auditory cortex?

A
  1. hair cells are arranged tonotopically along membrane with higher frequencies closest to the ossicles and windows
  2. APs project to the cochlear nucleus
  3. signals transmit up to the medial geniculate body as well as contralaterally to the superior olivary nucleus – creates lag to assist in sound location/intensity
  4. projection to primary auditory cortex and association areas via auditory radiations
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13
Q

Overview of the vestibular system + vestibular pathways

A
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14
Q

Physiology of the blood brain barrier

A

blood brain barrier consists of:

  • continuous layer of endothelium with tight junctions
  • pericytes – produce basement membrane
  • astrocyte end feet

only lipophilic substances and those with active transport mechanisms are able to cross, BBB can be compromised in pathological conditions or at circumventricular organs

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15
Q

Overview of neurological embryology

A
  1. nervous system develops from ectoderm via formation of the neural plate induced by chemicals released from the notochord
  2. invagination to form neural tube and release of neural crest cells (PNS, melanocytes, head connective tissue, pia/arachnoid, Schwann, chromaffin)
  3. closure of neural tube
  4. primary vesicle stage – rhombencephalon, mesencephalon, prosencephalon
  5. secondary vesicle stage – myelencephalon, metencephalon, mesencephalon, diencephalon, telencephalon
  6. mitotic activity in ventricular zone with migration of neurons along radial glia forming cortical layers in descending order (inside out)
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16
Q

Types of brain infections and routes of transmission

A

meningitis = inflammation of the meninges

encephalitis = inflammation of brain parenchyma

Routes of transmission:

  • haematogenous
    • crossing blood-brain barrier = encephalitis
    • crossing blood-CSF barrier = meningitis
  • direct spread from adjacent sites such as the sinuses, mastoid, skull fractures
  • iatrogenic
  • neural spread of viruses
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17
Q

Common causative organisms of meningitis

A

bacteria: E. coli, Group B Streptococcus, H. influenzae, N. Meningitidis, S, pneumoniae
viruses: HSV, adenovirus, HIV

infection of Neisseria meningitidis = meningococcal

  • 12 serogroups, most common are ABCWY, B approx. 50% of cases
  • vaccinations available – B, C, ACWY
  • can manifest as meningitis, meningococcaemia or a combination
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18
Q

Clinical signs of meningitis

A

positive Kernig’s sign:

  • flex hip and knee 90°
  • extension of the knee should be difficult/painful

positive Brudzinski’s sign:

  • passive flexion of the neck results in flexion of the knee/hip

QUAD of Danger:

  1. Headache
  2. Photophobia
  3. Neck stiffness (nuchal rigidity)
  4. Non-blanching rash → belly
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19
Q

Lumbar puncture findings in meningitis

A
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20
Q

Alar plate vs. basal plate in the spinal cord and brainstem

A

alar plate: dorsal side of spinal cord, afferent pathways, becomes lateral in brainstem

basal plate: ventral side of spinal cord, efferent pathways, becomes medial in brainstem

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21
Q

Structure of the retina

A

Retina has several cellular layers:

  • photoreceptors which convert photons → action potentials
    • rods – night vision, much more sensitive to light but monochromatic
    • cones – colour vision and visual acuity, three different types (red, blue, green)
  • interneurons for regulation/modulation
  • ganglion cells are output cells, axons form the optic nerve

macula lutea = centre of field of vision

fovea = centre of macula, area of highest visual acuity

optic disc = area with no photoreceptors where optic nerve leaves

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22
Q

Visual pathways

A
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23
Q

Outline of the pupillary eye reflex

A
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24
Q

Role of the MLF in conjugate gaze

A

Horizontal conjugate gaze is mediated by the frontal eye field, typically the FEF mediates movement of the eyes in the contralateral direction (left FEF = eyes moving to patients right)

  1. fibres from FEF travel to pons and decussate to contralateral PPRF
  2. interneurons communicate between PPRF and abducens nucleus
  3. two projections from abducens nucleus:
  • ipsilateral lateral rectus via CN6
  • contralateral oculomotor nucleus via MLF, controls medial rectus via CN3
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25
Q

Overview of neurotransmitter physiology

A
  1. Synthesis – peptide transmitters in cell body then transported, non-peptide transmitters are synthesised and stored in the nerve terminal
  2. Storage – occurs in vesicles within the active zone of the axon terminal
  3. Release – influx of calcium due to depolarisation triggers calcium dependent exocytosis
  4. Receptor binding – receptors on postsynaptic neuron may be rapid ionotropic (ligand gated ion channels) or slow metabotropic (second messengers)
  5. Degradation – reuptake into neurons and glia, enzymatic breakdown of active component
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26
Q

Overview of major motor pathways

A

Corticospinal tract

carries motor signals from M1/SMA/PMA to LMNs in the spinal cord

  1. primary neuron is an UMN originating in the motor cortices
  2. travels down through internal capsule – genu and anterior portion of posterior limb (FAL)
  3. decussation of some fibres at the pyramidal decussation creates two pathways:
  • lateral CST: 90% of fibres decussate in medulla and continue contralaterally in lateral SC
  • anterior CST: 10% of fibres remain ipsilateral and continue down in the anterior SC before later decussating at the level they innervate via the ventral white commissure
  1. synapse onto secondary neuron which is LMN in the ventral horn of the spinal cord

Corticobulbar tract

Carries motor signals from M1/SMA/PMA to LMNs in motor cranial nerve nuclei

  1. primary UMN from motor cortices travels down through genu of internal capsule
  2. synapse onto secondary LMN in motor cranial nerve nuclei, most of these nuclei are supplied bilaterally from the left/right CBT with two exceptions
  • facial: upper facial nuclei have bilateral innervation, lower nuclei contralateral only
  • hypoglossal: primarily contralateral innervation

Other non-pyramidal pathways include:

  • vestibulospinal – vestibular nuclei project to spinal cord for balance/posture
    • medial for bilateral head/neck control
    • lateral for ipsilateral proximal muscles
  • reticulospinal – two opposing pathways ipsilaterally control lower limb posture/walking
    • pontine/medial activates extensors
    • medullary/lateral inhibits extensors
  • rubrospinal – from red nucleus, complementary pathway to CST with unclear role
  • tectospinal – superior colliculus projects to SC to coordinate head/neck in visual reflexes
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27
Q

Overview of major sensory pathways (DCML and STT)

A

Dorsal column medial lemniscus – major sensory pathway for fine touch and proprioception

  1. primary sensory neurons with cell bodies in dorsal root ganglia enter the spinal cord through the dorsal roots and form the ascending dorsal columns (gracile/cuneate fasciculi)
  2. synapse onto secondary neurons in dorsal column nuclei of medulla
  3. secondary neurons decussate as the internal arcuate fibres before travelling up to the thalamus as the medial lemniscus
  4. synapse onto tertiary neurons in the VPL nucleus of the thalamus which continue up to S1

Spinothalamic tract – sensory pathway for pain and temperature

  1. primary sensory neurons with cell bodies in dorsal root ganglia enter spinal cord via dorsal roots and synapse in dorsal horn at same level (or slightly above/below via Lissauer’s tract)
  2. secondary neuron immediately decussates through ventral white commissure and ascends in the STT of the lateral funiculus
  3. synapse onto tertiary neuron in the VPL nucleus of the thalamus before continuing to S1

Fibres within the STT also have a number of additional cortical connections

  • reticular formation – alertness due to pain
  • midbrain – periaqueductal grey for descending pain modulation
  • hypothalamus – SNS response to pain
  • limbic system – emotional response to pain
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28
Q

Major Sensory Pathways (SCT and TTT)

A

Spinocerebellar tract – unconscious proprioception involved in cerebellar function

  1. primary sensory neurons synapse in dorsal horn of spinal cord
  2. secondary neurons ascend to ipsilateral cerebellum via two pathways:
  • information from golgi tendon organs travel up ipsilaterally through dorsal SCT and inferior cerebellar peduncle
  • information from muscle spindles decussates and ascends through the ventral SCT contralaterally before decussating again in the brainstem and entering the ipsilateral cerebellum via the superior peduncle

Trigeminothalamic tract – sensory information from the face

  1. primary sensory neurons with cell bodies in trigeminal ganglia enter the brainstem and synapse in one of three sensory nuclei
  • mesencephalic (midbrain): proprioception
  • principal sensory nucleus (pons): fine touch
  • spinal trigeminal nucleus (medullar): pain and temperature
  1. secondary neurons decussate and ascend through the TGT and synapse on tertiary neurons in the VPM nucleus of the thalamus
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29
Q

Classification + causes of stroke

A

ischaemic (80%)

  • embolism, thrombosis, systemic hypotension, cerebral venous sinus thrombosis

haemorrhagic (20%)

  • intracerebral – bleeding within the brain due to ruptured blood vessel
  • subarachnoid – bleeding outside the brain in subarachnoid space

commonly due to hypertension, bleeding disorders, aneurysm, trauma

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30
Q

Cellular pathophysiology of stroke

A

Neuronal cell death occurs due to excitotoxicity, extracellular glutamate is normally tightly regulated by sodium dependent reuptake systems in neurons and glia which become dysfunctional in ischaemia due to the loss of ATP

  1. ischaemia/hypoxia results in inability to maintain normal gradients
  2. accumulation of intracellular Na+ and extracellular K+ inhibits glutamate uptake systems and lack of ATP limits conversion of glutamate to glutamine in glia
  3. extracellular glutamate levels increase resulting in excess stimulation of NMDA receptors leading to excessive depolarisation – Na+ and Ca2+ entry
  • Ca2+ increases AMPA receptor expression, causing further excitation
  • excess K+ is not removed due to lack of ATP, disrupts membrane and leads to excessive depolarisation
  1. intracellular calcium overload is toxic and activates enzymes that initiate apoptosis
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31
Q

Common types of abnormal gait

A
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32
Q

Four parallel basal ganglia loops

A

motor loop – refining movement sequences

oculomotor loop – inhibition of saccades to focus via frontal eye field

limbic loop – reward and pleasure

cognitive loop – movement planning and decision making

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33
Q

Direct vs. indirect motor loops

A

Basal ganglia play a key role in motor planning and modulation of movement, the initiation and termination of a movement program is determined by two parallel pathways which are activated/deactivated by neurotransmitters in the striatum acting on medium spiny neurons

  • direct pathway – initiates movement, increased dopamine from SNpc
  • indirect pathway – terminates movement, increased ACh from within striatum

DIRECT PATHWAY

Activated due to dopamine from SNpc activating D1 neurons and inhibiting D2 neurons

  1. excitatory signals descends from motor cortex to D1 neurons
  2. D1 neurons inhibit the GPi/SNpr
  3. reduces inhibition by the GPi/SNpr on the PPN and thalamus
  4. increased output from PPN and thalamus resulting in greater SC output

INDIRECT PATHWAY

Activated due to ACh from large aspiny striatal neurons activating D2 neurons via M1 receptors and inhibiting D1 neurons via M2 receptors

  1. excitatory signal descends from motor cortex to D2 neurons
  2. D2 neurons inhibit the GPe
  3. reduces inhibition by the GPe on the STN
  4. increased excitatory output from STN on the GPi/SNpr
  5. greater inhibition from GPi/SNpr on thalamus and PPN
  6. decreased output from PPN and thalamus results in diminished SC output
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34
Q

Pathophysiology of Parkinson’s and Huntington’s diseases

A

Parkinson’s disease – unclear cause results in degeneration of dopaminergic neurons in the SNpc leading to a shift towards ACh in the striatum and the indirect pathway

  • major clinical signs: bradykinesia, rigidity, resting tremor
  • pharmacological management delayed as much as possible, mainstay is levodopa + carbidopa to restore dopamine in the striatum while limiting peripheral excess

Huntington’s disease – neurodegenerative disease that primarily affects GABAergic neurons of the indirect pathway and cholinergic aspiny neurons of the striatum

  • occurs due to autosomal dominant mutation in the huntingtin protein resulting in CAG repeats that produce a polyglutamine tail in the dysfunctional gene product
  • clinical signs: chorea, decreased muscle tone
  • managed with antipsychotics, antidepressants, counselling/support
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35
Q

Types of general sensory receptors

A
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36
Q

Types of dementia

A
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37
Q

Diseases of neural tube closure

A

Risk factors – folate deficiency, increased maternal age, family history, obesity, medications

rostral end: anencephaly

caudal end: spina bifida (varying degrees shown below)

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38
Q

Classification of hydrocephalus

A

Hydrocephalus = increased CSF within the cranial cavity

  • primary: non-communicating hydrocephalus caused by obstruction of normal CSF flow, causes may include congenital malformation (e.g. Chiari), inflammation, haemorrhage
  • secondary: communicating hydrocephalus due to atrophy of the brain with CSF filling the larger ventricular space
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39
Q

Common CNS neoplasms

A

GLIOMAS

  • glioblastoma* – high grade anaplastic glioma which can be either a very aggressive primary cancer or can develop secondarily from a lower grade glioma
  • astrocytoma* – relatively common with diffuse (worse) or localised (better) forms
  • oligodendroglioma* – slow growing but highly infiltrating with late presentation
  • ependymoma* – solid or papillary masses in ventricular system
  • ganglioglioma* – mixed CNS cancer with neurons and glia typically in superficial temporal lobe

OTHERS

  • medulloblastoma* – embryonal tumour most common in children, aggressive + rapid spreading
  • meningioma* – meningeal cancer may be idiopathic or associated with radiotherapy
  • schwannoma* – benign nerve sheath tumour often in vestibulocochlear nerve
40
Q

Considerations in spinal cord injury management

A

Different consequences/considerations depending on level of injury, major concerns include:

  • neurogenic shock: loss of sympathetic tone
  • autonomic dysreflexia: loss of inhibitory spinal signals can result in SNS overstimulation causing uncontrolled hypertension
  • respiratory compromise: impairment of muscles of breathing
41
Q

Functional divisions of the cerebellum and their afferent/efferent pathways

A

vestibulocerebellum = floculonodular lobe

role: position of head in space and subsequent maintenance of balance

  1. vestibular information relayed via CN8 and vestibular nuclei
  2. enters cerebellum and relayed to vestibulocerebellum via deep nuclei
  3. efferents travel back to deep nuclei as well as to vestibular nuclei (vestibulospinal tract) and reticular formation (reticulospinal tract)

spinocerebellum = vermis + paravermal zone

role: proprioception of the trunk to maintain balance/posture

  1. input from ipsilateral SCT via inferior (ventral SCT) and superior (dorsal SCT) peduncles
  2. relayed to spinocerebellum via deep cerebellar nuclei
  3. efferents travel out to contralateral motor cortices to control muscle movements ipsilateral to the initial input

cerebrocerebellum = lateral lobes

role: planning of movement patterns for the cortex

  1. information from contralateral cortex descends and decussates in pons
  2. enters via middle peduncle and relayed to lateral hemispheres by deep nuclei
  3. efferents travel out via superior peduncle, decussate in pons and relayed to contralateral motor cortices via thalamus
42
Q

Types of headache

A
43
Q

DSM criteria of schizophrenia

A

Schizophrenia is a psychiatric disorder characterised by severe disturbance in perception of reality including thinking, language, behaviour

The DSM criteria include:

  • at least two of the following for one month: delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour, negative symptoms
  • level of functioning is significantly lowered
  • continuous signs of disturbance for at least 6 months
  • no other cause – other psychiatric disorder, substance abuse, medical condition

positive symptoms – delusion, hallucination, disorganised speech/thought

negative symptoms – anhedonia, avolition, alogia, asociality, blunted affect

often coincides with cognitive and mood dysfunction as well

44
Q

Dopamine hypothesis of schizophrenia

A

It is believed that dysregulation of dopamine signalling plays a significant role in the pathogenesis of schizophrenia, this is supported by the dopamine inhibiting effects of most antipsychotic medications

Different dopaminergic pathways are thought to be responsible for different symptoms

  • mesolimbic: hyperactivity = positive symptoms (D2)
  • mesocortical: hypoactivity = negative symptoms (D1)
  • nigrostriatal: extrapyramidal side effects
  • tuberoinfundibular: hyperprolactinaemia side effects
45
Q

Risk factors for schizophrenia

A
  • modifiable* – substance use/abuse
  • non-modifiable* – genetics, FHx, paternal age, obstetric complications, childhood trauma, migrant status, urban upbringing
46
Q

Side effects of antipsychotic medications

A

Extrapyramidal side effects – primarily associated with typical or first-generation antipsychotics, these are associated with blockade of D2 receptors in the nigrostriatal pathway (ADAPT)

  • acute dystonia
  • akathisia
  • Parkinsonism (resting tremor, bradykinesia, cogwheel rigidity)
  • tardive dyskinesia

Hyperprolactinaemia – from blockade of the tuberoinfundibular pathway resulting in increased release of prolactin, causes galactorrhea, infertility, menstrual dysfunction, erectile dysfunction

Metabolic side effects such as increased appetite, weight gain, insulin resistance, obesity and type 2 diabetes mellitus are more associated with atypical antipsychotics

Cardiovascular disease including myocarditis, arrhythmias, hypertension

Clozapine has a number of specific side effects that need to be closely monitored particularly agranulocytosis, seizures, and CNS depression

47
Q

Common types of delusions

A

Persecutory – affected person feels they are being harassed/stalked/conspired against

Delusion of grandeur – heightened sense of greatness or influence

Delusional jealousy – belief that a spouse or partner is being unfaithful

Delusion of control – belief that somebody else is in control of one’s behaviour/thoughts

Delusion of reference – thinking everything is related to them e.g. people talking about them

48
Q

DSM criteria of depression

A

Major depressive disorder (MDD) = mental disorder characterised by a pervasive low mood and loss of interest in normally enjoyable activities

The DSM criteria include 5 or more of the following 9 symptoms in the same 2-week period:

  • depressed mood
  • loss of interest or pleasure
  • change in weight/appetite
  • insomnia or hypersomnia
  • psychomotor agitation or retardation
  • loss of energy or fatigue
  • feelings of worthlessness/guilt
  • impaired concentration
  • thoughts of death or suicidal ideation/attempts

Mnemonic is SIGECAPS – sleep changes, interest, guilt, energy, cognition/concentration, appetite, psychomotor, suicide

Persistent depressive disorder (PDD/dysthymia) = mood disorder consisting of symptoms of MDD persisting for at least two years in adults or one year in children/adolescents

Postpartum depression = symptoms of MDD arising within one month of parturition, may be associated with hormonal imbalances

49
Q

Pathophysiology of depression

A

As with other psychiatric conditions, the underlying cause of depression is likely to be a complex interplay between biological, environmental, and psychological factors, there are several theories of physiological dysregulation thought to be involved:

  • monoamine deficiency theory: dysregulation of neurotransmitter systems particularly serotonin, dopamine, and noradrenaline – each of these can be linked to groups of symptoms and have a number of interactions with each other
  • HPA axis dysfunction: chronic activation of the HPA axis is implicated, cortisol acts in a feedback loop with the anterior pituitary and hypothalamus + evidence of hippocampal atrophy which may be the basis of dysfunction
    • associated with neurotransmitter systems
    • increased risk of cardiovascular disease
  • second messenger system dysfunction
50
Q

Antidepressant medications and side effects

A
51
Q

DSM criteria of bipolar affective disorder

A

Bipolar disorder = mental disorder characterised by episodes of depression and abnormally elevated mood also known as mania/hypomania

  • mania: euphoria, grandiosity, pressured speech, impulsivity, diminished need for sleep, may include delusion or hallucinations
  • hypomania: manic symptoms for at least four days but without functional decline and no psychosis
  • depressive symptoms are in line with those of major depressive disorder

bipolar I – at least one manic episode, may be preceded or followed by episodes of depression or hypomania but these are not necessary for diagnosis

bipolar II – one or more episode of hypomania and one or more episode of MDD

cyclothymia – history of hypomania and depressive symptoms (not qualifying for MDD) over at least two years

52
Q

Manic symptoms

A

(DIGFAST)

Distractibility

Impulsivity

Grandiosity

Flight of ideas

Agitation (psychomotor)

Sleep (decreased need)

Talkativeness or pressured speech

53
Q

Structures of the limbic system

A

The limbic system is a grouping of brain structures which supports a variety of structures including emotion, behaviour, and memory

Limbic structures – amygdala, hypothalamus, hippocampus, fornix, nucleus accumbens

54
Q

Types of memory

A

Two types of memory:

  • explicit: semantic = facts, episodic = experiences
  • implicit = skills and procedural memory

Stages of memory formation:

  • sensory memory holds sensory information for less than one second to help form a smooth sense of the world around you
  • short term or working memory allows recall for seconds to a minute without rehearsal but has limited capacity, able to be measured
  • long term memory theoretically has unlimited capacity and is believed to be stored in neurological circuits throughout the entire brain
55
Q

Overview of Papez’s circuit

A

Papez’s circuit = hypothesised limbic circuit for memory consolidation

  1. Entorhinal cortex receives input from all cortical regions and projects to hippocampus
  2. Axons from hippocampus form the fornix which spits into two pathways at the anterior commissure
  • precommissural fibres – septal area + NAc, reward component of memory
  • postcommissural fibres – 90% of fibres travel to mamillary bodies which are a hypothalamic nucleus, these project to thalamus via mammillothalamic tract
  1. Thalamus projects to cingulate cortex, from here the memory can either return to the beginning of the loop for layering/consolidation or is stored by some means
56
Q

Amygdala pathways

A

The amygdala consists of a number of nuclei which are thought to be key in linking sensory perception with emotional responses – receives input from sensory fields, insula, memory

Two major outputs:

  • amygdalofugal – decision about movement via learned responses of reward/punishment
  • stria terminalis – output to hypothalamus for visceral activation when anxious/stressed
57
Q

Regions of prefrontal cortex

A

Dorsolateral – executive functions including decision making, working memory and planning

Ventromedial – emotional responses, self-control, morality

58
Q

Psychosocial and non-pharmacological interventions

A

Psychosocial interventions

Cognitive behavioural therapy (CBT) is based on the assumptions that mood disorders are accompanied by systematic distortions in thinking and that this interpretation events influences how they affect us

Techniques include:

  • challenging negative beliefs
  • monitoring thoughts, feelings, and behaviours
  • activity scheduling
  • behavioural experiments to disprove negative predictions

Other forms of therapeutic counselling include:

  • psychodynamic therapy – interpretation of mental and emotional processes to help patients find patterns in their emotions/thoughts/beliefs
  • family therapy – focus on improving communication and resolving conflicts

Non-pharmacological interventions

  • electroconvulsive therapy (ECT) = uses electric current to induce seizures as a treatment for severe depressive and psychotic symptoms
  • transcranial magnetic stimulation (TMS) = similar premise to ECT using magnetic fields to stimulate neural circuits within the brain
  • vagal nerve stimulation (VNS) = stimulator device implanted in the chest sends regular pulses of electricity to the brain via the vagus nerve to influence neural networks
59
Q

DSM criteria of delirium

A

The DSM criteria for delirium includes:

  • disturbance in attention and awareness/orientation
  • develops over a short period of time and fluctuates throughout the day
  • decline in cognitive functioning
  • not explained by another neurocognitive disorder with evidence that the disturbance is a direct consequence of another medical condition or medication/drug use/withdrawal
60
Q

Differentials for delirium

A

Toxicity – medications, illicit drugs

Metabolic disturbance – hypoglycaemia, hyperglycaemia, ketoacidosis, electrolyte imbalance

Neurological – brain tumour, TIA, stroke, meningitis/encephalitis

Hypoxia or hypercapnia

Acute urinary obstruction

Thyrotoxicosis or myxoedema coma

61
Q

Serotonin syndrome

A

Group of symptoms which are associated with use of multiple serotonergic medications or drugs which can be a medical emergency – results from excess serotonin in the CNS

  • signs/symptoms: high body temperature, agitation, sweating, mydriasis, seizures, rhabdomyolysis
  • treatment involves discontinuing medications, serotonin antagonists, active cooling
62
Q

Overview of personality disorders

A

Personality disorders are pervasive and inflexible patterns of experience and behaviour that deviate markedly from expectations of an individual, categorised into three types:

  • eccentric/erratic
  • emotional/reactive
  • rigid functioning

e.g. borderline personality disorder, 10 main criteria (5 needed) including frantic efforts to avoid abandonment, identity disturbance, mood swings, inappropriate intense anger, impulsivity

63
Q

Types of anxiety disorders

A
64
Q

Criteria for involuntary admission

A

Mental illness = presence of one or more of the following:

  • delusions
  • hallucinations
  • serious disorder of thought form
  • severe disturbance of mood
  • sustained irrational behaviour suggesting any of the above symptoms

Person with mental illness is somebody exhibiting a mental illness with reasonable grounds to believe that temporary care and control are necessary for the safety of the person and others

Mentally disordered person is someone who has behaviour so irrational that temporary care and control is necessary to protect them or others from serious harm

Involuntary admission is a complex process initiated if a person is believed to be mentally or disordered and there are no other less restrictive means of care available

  • involves multistep series of evaluations by medical professionals
  • review by mental health inquiry + tribunal
65
Q

What is the 1st cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
66
Q

What is the 2nd cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
67
Q

What is the 3rd cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
68
Q

What is the 4th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
69
Q

What is the 5th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
70
Q

What is the 6th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
71
Q

What is the 7th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
72
Q

What is the 8th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
73
Q

What is the 9th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A

by Arch –> not sure about pharynx deviation (that aahh test is for uvula CN 10)

CN 9 test = gag reflex/swallowing water

palsy = loss of taste/sensation to posterior 1/3 of tongue + can’t swallow properly

74
Q

What is the 10th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
75
Q

What is the 11th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
76
Q

What is the 12th cranial nerve? Describe the:

  • Name
  • Location of the nuclei in the brainstem
  • Function
  • How to test it
  • Exit point of skull
  • Nerve palsy signs
A
77
Q

Exit points of the skull for each Cranial nerve

A
78
Q

Label the CN nerves

A
79
Q

Cerebral circulation supplies and findings if infarcted of:

Internal Carotid (ICA)

A
80
Q

Cerebral circulation supplies and findings if infarcted of:

ACA

A
81
Q

Cerebral circulation supplies and findings if infarcted of:

MCA

A
82
Q

Cerebral circulation supplies and findings if infarcted of:

PCA

A
83
Q

Cerebral circulation supplies and findings if infarcted of:

Lenticulostriate

A
84
Q

Cerebral circulation supplies and findings if infarcted of:

ACA-MCA Watershed

A
85
Q

Cerebral circulation supplies and findings if infarcted of:

MCA-PCA Watershed

A
86
Q

BRAINSTEM circulation supplies and findings if infarcted of:

PCA

A
87
Q

BRAINSTEM circulation supplies and findings if infarcted of:

PICA

A
88
Q

BRAINSTEM circulation supplies and findings if infarcted of:

Basilar Artery

A
89
Q

BRAINSTEM circulation supplies and findings if infarcted of:

AICA

A
90
Q

BRAINSTEM circulation supplies and findings if infarcted of:

Vertebral + Spinal Arteries

A
91
Q

BRAINSTEM circulation supplies and findings if infarcted of:

Superior Cerebellar Artery

A
92
Q

Name the structures

A
93
Q

Name the structures

A
94
Q

Name the structures

A
95
Q

Pathogenesis and symptoms of Schizophrenia

A
96
Q

Indirect Vs Direct Pathway in Parkinson’s and Huntington’s

A

EOP 1 (16 decks)

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