Neuro to learn Flashcards

1
Q

causes of OCD

A
  • basal ganglia re-entranty circuits
  • PANDA
  • low seratonin (think anxiety is treated with SSRIs)
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2
Q

PANDA

A

paediatric autoimmune neuropsychiatric disorder associated with streptococcal infection

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3
Q

compulsions

A

are motor acts associated with obsessions

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4
Q

Treatment of PTSD

A

Biological

  • SSRIs
  • Maybe short term benzodiazepines

Psychological

  • CBT
  • Eye movement desensitization reprocessing therapy

Social

  • Charities are particularly active, such as ‘Help for Heroes’
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5
Q

mood disorders

A

depression

bipolar 1 and 2

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6
Q

peripheral modulation of pain

A

substantia gelatinosa

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7
Q

adjustment reaction vs depression

A
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8
Q

Features of Mania (opposite of depression)

A

Elated Mood

Increased energy

Pressure of speech

Decreased need for sleep

Flight of ideas

Normal social inhibitions are lost

Attention cannot be sustained

Self esteem is inflated, often grandiose

May have psychotic symptoms

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9
Q

Physical health differentials: Mania

A

Iatrogenic e.g. steroid induced

Hyperthyroidism

Infection e.g. syphyllis

Head injury

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10
Q

brain system involved in anxiety disorders

A

limb system

  • hippocampus
  • fornix
  • amygdala
  • pre-frontal cortex
  • cingulate gyrus
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11
Q

Brain structures involved in mood disorders

A

• Limbic system

  • Frontal lobe
  • Basal ganglia
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12
Q

the limbic system function

A

memory

emotion

motivation

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13
Q

Basal ganglia functions

A

motor and psychological

Motor function; malfunction of the basal ganglia are implicated in neurological illnesses such as

  • Parkinson’s disease
  • Wilson’s disease
  • Huntington’s disease

Psychological function:

  • Emotion
  • Cognition
  • Behaviour
  • Reveal Answer
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14
Q

The two main neurotransmitters for depressive disorders are:

A

A

Serotonin - raphe magnus

Noradrenaline- locus coeruleus (pons)

both decreased in depression

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15
Q

Physical health differentials: depression

A
  • thyroid dysfunction
  • vitamin B12 deficiency
  • Chronic disease e.g. renal, CVS & liver failure
  • Anaemias
  • Substance misuse
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16
Q

Biological treatment of bipolar depression

A

Can use antidepressant – but ONLY with mood stabiliser cover.

  • ECT
  • Lithium
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17
Q

Maintaining stability in bipolar disorder

A

Biological

Mood stabilisers e.g. lithium, sodium valproate- shouldn’t be used on women of a child bearing age (anticonvulsant)

Antipsychotic (used as a mood stabiliser e.g. Quetiapine)

Psychological

Psychoeducation re. bipolar affective disorder.

CBT – to help prevent relapses

Social

Consideration of BPAD on employment e.g. shift work.

Involvement of family, education of family etc.

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18
Q

psychosis is the presence of

A

hallucinations (perception without stimulus) and delusions (fixed, false beliefs that conflict with reality)

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19
Q

hypogognic

A

hallucinations whilst falling asleep

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20
Q

hypnopompic

A

hallucinations when waking uo

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21
Q

First Rank Symptoms of schizophrenia

A

SAD PT

Somatic hallucinations

Auditory hallucinations

Delusional perceptions

Passivity experiences

Thought withdrawal, broadcast or insertion

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22
Q

positive symptoms of psychizophrenia

A

Delusions, hallucinations, thought disorder, lack of insight

Added symptoms

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23
Q

Pathophysiology of Schizophrenia

A

Dopamine pathways

Brain changes

Limbic system

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24
Q

schizophrenia dopamine pathways involvement

A

Mesolimbic- dopamine overactive

Mesocortical- dopamine underactive

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25
Q

Brain changes in schizophrenia

A
  • Enlarged ventricles
  • Reduced grey matter
  • Decreased temporal lobe volume (auditory hallucinations)
  • Reduced hippocampal formation, amygdala, parahippocampal gyrus and prefrontal cortex
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26
Q

treatment of schizophrenia

A

typical and atypical antipsychotics

typical - antagonise D2 receptors in all dopamine pathways (Parkinsonism side effect)

atypical

  • Lower affinity for D2 (dopamine) receptors
  • Milder side effects as dissociate rapidly from D2 receptor
  • Also block 5HT2 (serotonin) receptors – less parkinsonism
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27
Q

side effects of antipsychotics

A

hyperprolactinaemia

  • Dopamine normally inhibits prolactin release from the pituitary.
  • DA antagonists, which lower DA lead to loss of DA’s inhibitory function, and therefore increased prolactin levels.
  • This can lead to: amenorrhoea, galactorrhoea, decreased fertility, reduced libido and long term can lead to osteopenia/osteoporosis
28
Q

Spinal nerve split to form the

A

ventral ramus (suppling brachial and lumbosacral plexus) and the dorsal ramus (supplies intrinsic muscles of the back)

29
Q

important disorders related to neural crest cells

A

Hirshprungs- certain segment sof the gut will have no enteric nervous system- constipation

Di Georges- not T cell education in the thymus

30
Q

Glucose lactate shuffle

A
  1. Astrocyte stores glycogen
  2. Astrocyte produce lactate from the breakdown of glycogen
  3. Lactate then shuttled across with H+ via the MCT1 transporter on the astrocyte and the MCT2 transporter on the neuron
  4. Lactate is then converted to pyruvate
  5. Pyruvate metabolism releases ATP which can be used as an energy source of the neurone
31
Q

ionotropic glutamate receptors

A

integral ion channel – activation of receptor, ion channel opens, inward movement of Na+  depolarisation

AMPA receptors

Permeable to Na and K+

NMDA receptors

Permeable to Na ,K+ and Ca2+

Calcium permeability important

Kainate receptors

Permeable to Na and K+

Reveal Answer

32
Q

Glycine’s role in the stretch reflex

A

The inhibitory relay neurone then releases glycine which inhibits the motor neurone to the antagonist muscles (hamstring) therefore allows the hamstrings to relax

33
Q

neurofibrillary tangles made out of

A

Tau protein

usually stabilise microtubules

34
Q

lewy bodies made out of

A

protein alpha-synuclein, a cytoplasmic protein associated with synaptic vesicles.

35
Q

frontotemporal dementia pathophysiology

A

FTD-tau

FTD-U (ubiquitin)

36
Q

classification of FTD

A

3 behavioural presentations of FTD

Apathetic

Disinhibited

Stereotypic

37
Q

The…………… is an important muscle, as it opens the eye and is innervated by cranial nerve III.

A

levator palpebrae superioris (LPS)

38
Q

smooth muscle that originates from LPS undersurface, called the ……………..is innervated by postganglionic sympathetic axons from the superior cervical ganglion.

A

superior tarsal muscle

–> causes ptosis if sympathetic innervation affected e.g. pancoast tumour

39
Q

L3 myotome = major input to

A

quadriceps

40
Q

L5 myotome supplies the

A

hamstring

41
Q

patellar reflex

A

(L3 level- L3 myotome = major input to quadriceps)

  1. Patellar ligament in tapped by tendon hammer
  2. Stretching of fibres of the quadriceps is detected by muscle spindles found within the quad muscle
  3. Muscle spindles detect muscle length= stretch
  4. Stretched detected by muscle spindle is conveyed to the spinal cord via first order sensory afferent (cell body found in the dorsal root ganglion)
  5. This first order sensory afferent enters the dorsal horn and projects down to the ventral horn and synapses onto a lower motor neurone
  6. LMN sends its axon down into the ventral root and down to the quadriceps muscle itself causes twitch

What about the hamstrings? Need them to stop antagonising the action of the quads

If the quads are contracting this would cause the hamstring to contract and this would result in no movement at all  agonist+ antagonist contraction= no movement

Therefore:

  1. L5 myotome supplies the hamstring
  2. First order sensory neurones sending info from the muscle spindle in the quadricep descends down from L3 to L5 and synapse with inhibitory interneurons
  3. Inhibitory interneurons inhibit LMN supplying the hamstring (selective inhibition of hamstrings)
  4. Therefore antagonists effect of hamstrings muted and the patellar reflex can cause full extension at the knee
42
Q

Nucleus ambiguous

A

collection of cell bodies of LMN that will distribute along the vagus nerve and innervates muscles of the vocal cords and pharynx)

  • Bilateral innervation
  • Required because nucleus ambiguous controls swallowing necessary for survival
43
Q

Monosynaptic reflex arc can help us understand pahtophysiology of hypertonia and spaticity

e.g. in someone who has had a stroke

A
  1. Cortical lesion e.g. stroke destroys excitatory corticospinal tracts and the descending inhibitory inputs
  2. Initially lower motor neurone will go into a state of ‘spinal shock’
    • Frequency of AP running along LMN will decrease significantly
    • Therefore tone of muscle supplied by this LMN will increase
  3. As time goes on the LMN starts to wake up
    • Realises it still has the excitatory input of the muscle spindles (sensory afferents)
  4. However, loss of CST- therefore no voluntary movements
  5. Lost descending inhibitory influences
  6. Therefore breaks have been taken off LMN, therefore it will fire off more frequent AP, leading to more frequent muscle contracts = increased muscle tone
  7. Loss of net inhibition therefore increase excitation
44
Q

why do lacunar infarcts affect the brain, upper and lower limb equally

A

This is due to fibres from the corticospinal tract showing less somatotopic organisation in the internal capsulee.g. face and lower limb fibres mixes

45
Q

how does the cerebellum decide which order joints need to flex/extend?

A

Receives this info from the primary sensory cortex and the spinocerebellar tract (information from proprioceptors in the muscles up the spinal cord into the cerebellum)

Cerebellum than communicates back to the primary motor cortex (via the thalamus)

46
Q

why do signs and symptoms of cerebellum lesions occur on the ipsilateral side?

A

double decussation of nerve fibres

47
Q

role of Lissauer’s tract in browns-sequard syndrome

A

explains why spinothalamic and dorsal column modalities can be lost at different spinal cord levels

  • axons within Lissauer’s tract are first order sensory neurones which ascend around 2 segments before synapse onto 2nd order
48
Q

locked in syndrome

A

if cortical spinal tracts not suppplied by the pontine branches on the basilar artery

  • Cortical spinal tract death –>no movement
  • Midbrain still supplied so can move eyes
    *
49
Q

where are berry aneurysms most commmon

A

posterior communicating arteries

50
Q

medication for stabilisation of subarachnoid

A

nimlodopine - pfrevent vasospasm

51
Q

Clinical signs of raised ICP are best predictors of when to delay an LP:

A

Decreasing consciousness

Brainstem signs

Recent seizure

CT head can be useful to find contraindications to doing an LP

But a normal CT may not mean that an LP is safe to perform

52
Q

meningitis

A

tetracyline (ceftrioxone)

53
Q

outline how the RF keeps us awake

A

Inputs to the RF which keeps us conscious

  • Excitatory (cholinergic) input from the cerebral cortex to the reticular formation in the brainstem
  • Sensory input (e.g. first/2nd order sensory neurones from the body) to the RF

Outputs from the RF to the cortex to keep us conscious

  • RF provides outputs which have to pass the thalamus (cholinergic synapse) and project up to the cortex
    • Glutaminergic projections up to the cortex
  • RF also provides outputs which pass the hypothalamus (cholinergic synapse) which project up to the cortex
    • Histinermergic projections up to the cortex
  • RF sends outputs to the basal forebrain (cholinergic synapse) nuclei which also project up to the cortex
    • Cholinergic projections up to the cortex

Both input and output projections are excitatory- positive feedback loop (cholinergic – ACh transmitter)

Transmitters released in the cortex maintain awake fullness

54
Q

distal MCA occlusion: Superior division problems

A

Supplies the lateral frontal lobe e.g. primary motor cortex and the Broca’s area

Examples of superior division problems

  • Contralateral face and arm weakness
  • Broca’s (Expressive) aphasia
    • Only if occurs on the LHS
55
Q

distal MCA occlusion: Inferior division problems

A

Examples of inferior division problems e.g. primary sensory cortex and Wernicke’s area

  • Contralateral face and arm loss of sensation
  • Wernicke’s aphasia
  • Homonomous hemianopia if both optic radiations are damaged or a quadrantanopia if just one radiation is affect
    • Without macula sparing (only macula sparing if PCA stroke)
56
Q

which structure in the brainstem ensures coordinated eye movement

A

Medial Longitudinal Fasciculus

57
Q

A 26-year-old female presents with double vision when looking to her left-hand side. She is normally fit and well except for an episode of paraesthesia in her left arm 6 months ago and right foot 2 years ago. Both of which resolved spontaneously within 24 hours and no medical attention was sought at the time.

suggets a diagnosis

A

multiple sclerosis

58
Q

what is used to elicit a difficult reflex

A

Jendrassik maneuver is a medical maneuver wherein the patient clenches the teeth, flexes both sets of fingers into a hook-like form, and interlocks those sets of fingers together. The tendon below the patient’s knee is then hit with a reflex hammer to elicit the patellar reflex.

59
Q

gracile fasciculus

A

dorsal column- lower body

60
Q

cuneate fasciculus

A

dorsal column- upper body

61
Q

The Romberg test

A

is a test of the body’s sense of positioning (proprioception), which requires healthy functioning of the dorsal columns of the spinal cord. The Romberg test is used to investigate the cause of loss of motor coordination (ataxia).

62
Q

Which three ligaments would your spinal needle have to traverse in order to perform the lumbar puncture successfully?

A

Supraspinous ligament

Interspinous ligament

Ligamentum flavum

63
Q

A 45 year old woman is admitted following a stab wound to her back. She has sustained a complete hemisection of the left side of her spinal cord at the level of L3.

Describe the pattern of SENSORY loss that would be expected. (3 marks)

A

Total sensory loss ipsilateral (left) L3 (1 mark)

Ipsilateral (left) dorsal columns L3/4 down (1 mark)

Contralateral (right) spinothalamic L4/5 down (1 mark)

64
Q

Q1 A 78-year-old man with a history of hypertension presents to A&E with new, sudden onset, unilateral weakness and a visual field defect. He has a CT scan which confirms the diagnosis as an acute, ischaemic stroke. His visual pathway is affected at area 4 on the diagram, what pattern of visual field defect will this have caused?

Bitemporal hemianopia

Left homonymous hemianopia

Right homonymous hemianopia

Left homonymous inferior quadrantanopia

Right nasal hemianopia

A

Left homonymous hemianopia

65
Q

cogwheel rigidity

A

sign of parkinsons

your muscle will be stiff, like in other forms of rigidity. But you might also have tremors in the same muscle when it’s at rest. Cogwheel rigidity can affect any limb, but it’s most common in the arms. It can affect one or both arms.