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A2 ME3031 NEURO > W9: Cerebral Hemispheres; SC & Periphery; Motor Control; Memory & Cognition; Sleep; Sensory Systems; Neuroradiology > Flashcards

W9: Cerebral Hemispheres; SC & Periphery; Motor Control; Memory & Cognition; Sleep; Sensory Systems; Neuroradiology Flashcards

1
Q

Frontal Lobe landmarks

A

Prefrontal Cortex

(4) Precentral Gyrus (Motor)
(44) (45) Broca’s Area

> BROCA’S APHASIA: missing small words

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2
Q

Parietal Lobe Landmarks

A

(3) (1) Postcentral gyrus (sensory)
(2)
- sup. parietal lobule: awareness of L 1/2 of body
- inf. lobule: global sensory area

> hemisensory neglect

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3
Q

Temporal Lobe Landmarks

A

(41) (42) Superior Temporal Gyrus: 1º Auditory Cortex

Wernicke’s Area (post) - dominant hemisphere
> WERNICKE’S APHASIA: fluent but meaningless

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4
Q

Occipital Lobe Landmarks

A

(17) 1º Visual cortex either side of calcacrine sulcus

(18) (19) visual assoc. areas: interpretation

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5
Q

Limbic Landmarks

A 
Cingulate
Hippocampus
Parahippocampal Gyrus
Amygdala
=> Memory formation + emotion
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6
Q

Describe the main fibre systems of the forebrain

A

White matter projections:

1) COMMISURAL: (L) to (R) corresponding
2) ASSOCIATION: unilateral. one area to another.

3) PROJECTION: cerebral cortex to subcortical centres
=> INTERNAL CAPSULE
> demse stroke (MCA)

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7
Q

Name the components of the basal ganglia and their function

A

CAUDATE NUCLEUS

LENTIFORM NUCLEUS

SUBSTANTIA NIGRA

=> control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, & emotion.

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8
Q

Arrangement of spinal tracts at the spinal cord

A

DORSAL COLUMN

CORTICOSPINAL

LATERAL SPINOTHALAMIC

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9
Q

DORSAL COLUMN

A

peripheral sensory to cerebral hemisphere; pseudounipolar | touch tactile vibration proprioception

  • 1º neurone => DRG (pseudounipolar) => DORSAL COLUMN
  • Synapse at Medulla oblongata nuclei (GM)
  • 2n Neurone: decussates => Thalamus (VPL)
  • 3n Neurone (VPL) => Post Central Gyrus (opposite side)
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10
Q

CORTICOSPINAL TRACT

A

voluntary skilled movements | cortex to muscles

  • 1n Neurone begins at (4) 1ºMC Precentral
  • PROJECTION travel down via CORONA RADIATA => IC
  • Midbrain: Ant. CRUX CEREBRI
  • Pons: anterior pontine nuclei
  • Medulla Ob: tracts form PYRAMIDS => DECUSSATE
  • Travel down anterior spinal cord as tracts
  • Synapses at appropriate level (GM) and exits the spinal cord
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11
Q

LATERAL SPINOTHALAMIC TRACT

A

Ascending sensory: pain + temperature

  • 1n GM /medulla synapse and exit at same level @ SC
  • 2n crosses to lateral column and travels up.
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12
Q

Name the components of a reflex arc.

A 
TENDON STRETCHED (monosynaptic):
intrafusal fibres stimulated
- sensory n. activated dorsal > GM > ventral horn > effector muscle

Flexor and extensor reflex (polysnaptic)
•PAIN > sensory neurone
• FLEXION + WITHDRAWAL via dorsal + inhibition via ventral
• crossed extensor to contralateral limb

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13
Q

Muscle tone lesions

A

UMN lesion = tone spasticity (corticospinal dmg) + LMN reflexes exaggerated but absent UMN reflexes + contralateral hemiparesis

*hypertonic
\+exaggerated LMN, nil UMN reflexes
\+ CLONUS
\+ upgoing babinski
\+ reduced power

LMN = flacidity
*hypotonic
+ downgoing babinski
+ HYPOREFLEXIA

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14
Q

Brown Sequard Syndrome

A

Herniated C3
>ipsilateral deficit

at level of lesion: LMN lesion symptoms
below level: UMN lesion symptoms

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15
Q

Explain what is meant by ‘readiness potential’

A

measure of activity in the motor cortex and supplementary motor area of the brain leading up to voluntary muscle movement. Pre-motor planning.

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16
Q

Name two disorders which may occur when the basal ganglia are damaged and the sites of damage

A

PARKINSONS DISEASE: substantia nigra degen. + subsequent loss of dopaminergic input to striatum
• HYPOKINESIA: slowness, difficult to make voluntary movements.
• ↑muscle tone + hand/jaw tremors

HUNTINGTON’S DISEASE: degen. of caudate and lentiform = loss of inhibitory effects of basal ganglia | Hereditary
• Hyperkinesia + dementia + personality disorders
• Charateristic chorea

17
Q

Outline the essential processes involved in motor learning

A

Motor learning occus in the cerebellum.

18
Q

List the symptoms which may be seen in patients with cerebellar disorders.

A

Disorder of coordination

Ataxia (which alcohol can depress further)

19
Q

Outline the role of the Limbic System in learning and memory

A

LIMBIC SYSTEM
+ Formation (hippo) storage (cortex) and access of memories (thalamus)
+ iNTEGRATION of inputs to make sense of situation
+ Reward/punishment

> HSV: hippocampal dmg = inability to form new LT mems

20
Q

Outline the differences between short term memory and long term memory

A

1) IMMEDIATE/SENSORY MEMORY
2) SHORT TERM => reverberating circuits; excitatory; vulnerable (seconds/hours)
3) INTERMEDIATE LT => undergoing chemical adaptation @ presynaptic terminal (⇈Ca influx = ⇈NT)

4) LT => structural: ⇈: NT release sites / Vesicles stored / Presynaptic terminals
+ ↑Amplitutde of graded membrane potential in post synapse.
=> LT POTENTIATION: established and rehearsed pattern of activity unique to that memory

• DECLARATIVE/EXPLICIT MEMORY: abstract/episodic/semantic @ HIPPO

• PROCEDURAL/REFLEXIVE/IMPLICIT MEMORY:
repition, motor memory acquired, rules @ CEREBELLUM

21
Q

Amnesias and how

A

RETROGRADE AMNESIA d/t thalamus dmg
-past loss; cannot access

ANTEROGRADE AMNESIA d/t perm. hippo dmg
- inability to form new LT

brought about by disruption to reverbation circuits required for short term memory

22
Q

Papez Circuit

A
  • essential in reverbation
  • parts of circuit associated w/ cortex areas resulting in unique multiple associations
FRONTAL  ⇔ sensory associated areas
⇕.      |       ⇕
CINGULATE GYRUS
⇕.      |.       ⇕
Anterior Thalamus.  |   Hippo 
⇧.                     |.     ⇩
MAMILLLARY BODY
23
Q

Associations & Pathologies of Memory

A

• Limbic + Olfactory

• Korsakoff’s Syndrome: B1 def d/t alcoholism
=> dmg to limbic therefore memory consolidation impaired

  • ALZHEIMER’S: cholinergic loss + hippo.
  • REM Sleep: Cholinergic neurones responsible for REM. dreaming reinforces weak circuits.
24
Q

Origin of sleep & molecules & regulation

A

Pons = inhibitiotiroy processes
Reticular Formation controls CONSCIOUSNESS: arousal and sleep centres.

Delta Sleep Inducing Peptide (CSF)

Adenosine: ⇧day; caffiene

MELATONIN: orexin (excit. NT - arousal)
(PINEAL GLAND - reg by suprachiasmatic nuclei - affected by light) therefore rhythmic

SEROTONIN: melatonin precursor. Reticular formation contain serotnergic neurones

25
Q

Explain the significance of the amplitude and frequency of EEG waves in terms of cortical activity

A

⇧Frequency w/ NEURONAL EXCITATION
Amplitude informs the strength of the pattern.

⇧Frequency = ⇩Amplitude Relationship

26
Q

4 Main EEG Types

A

α => relaxed, awake HIGH FREQ MED. AMPL.

ᵝ => alert, awake V. HIGH FREQ LOW AMPL.

ϴ => early sleep LOW FREQ ENORMOUS AMPLITUDE

δ => deep sleep LOWER FREQ HIGH AMPLITUDE

27
Q

Describe the typical pattern of a night’s sleep in an adult

A

1) SLOW ϴ, NON-REM
2) SLEEP SPINDLES: eye stops. short bursts, ⇧freq
3) SPINDLE DECLINE δ + +episodic bursts of high freq

4) δ waves
+ hippo activity
+metabolic drop
=> DEEP SLEEP/ SLEEP WALKING

=> (3) (2) rapidly w/ ⇧⇧amplitude
=> REM sleep

=> Rinse & Repeat

28
Q

Features of REM Sleep

A

⇧Frequency ⇩Amplitude (similar to ᵝ)

  • REM constitudes the concentrated periods at the end of sleep
  • increases in frequency and duration
    => new neurological connections + consolidation

*cholinergic dependent + inhibition of skeletal muscles via pons

29
Q

Sleep Disorders

A

NARCOLEPSY: abn orexin release from hypothalamus (pinneal gland)

nightmares: occur in REM

night terrors: deep sleep; children

SOMNAMBULISM: NREM, (4) deep delta, habitual + complex tasks, no recollection

30
Q

Explain the concept of sensory transduction

A

Transducted via 1º AFFERENT FIBRES

AB : long unmyelin.: TOUCH, PRESSURE, VIBR.

Aδ : short myelin. : COLD FAST PAIN PRESSURE

C: unmyelinated: warmth, slow pain

B: ipsilateral columns; cuneate + gracile nuceli synapse > decussate

adaptation of sensory terminals:
rapid (++ — ++ (removal)
slow AP gradually stops but stimulation continues

convergence: 2 neurones > neurone
* specific: same stimuli
* nonspec: 2 diff stimuli
* referred pain from visceral > somatic structures of same dermatome *

lateral inhibition: neighbouring inputs inhibited @ 2nd neurone = focussing

31
Q

Lesions of 1º afferent fibres

A

Aalpha & AB = ipsilateral loss of touch pressure and vibration

Aδ+C = contralateral loss of nociception and temperature

(think left C3 - brown sequard)

32
Q

Explain how tissue damage can lead to pain

A

free nerve endings stimulated by noxious stimuli via
Aδ+C
VRI receptors
local chemoreceptors: bradykinin; histamine; prostaglandins

=> depol => AP produced

+ segmental controls: gated AB activation inhibits Aδ+C (interneurone) via opiod-endorphin peptides
+ descending controls from PAG > ucleus raphe magnus > excitatory 5HT > inhibitiory interneurones of Aδ+C

33
Q

Explain why pain originating from the viscera can often result in sensation being referred to a somatic structure from the same dermatomes

A

convergence: 2 neurones > main dermatome neurone

* referred pain from visceral > somatic structures of same dermatome *

34
Q

Explain the mechanism of action of commonly used analgesic drugs.

A
  1. NSAIDS: sensitisation of prostaglandins inhibiting cyclo-oxygenase -| arachidonic acid -> prostaglandins
    ↓5htR sensitisation = ↓AP
  2. TENS: stimulate AB therefore stimulating gate theory => inhibition of Aδ+C
3. Opiods:
↓sensitisation of receptors = ↓AP
\+
block transmitter release (dorsal horn) via epidural transmission
\+
activation of PAD descending pathway
35
Q

MRI phases

A

T1-weighted

  • dark CSF + water
  • bright fat

T2-weighted

  • white CSF + water => oedema
  • fat is dark
36
Q

CT in Neuroradiology

A

Ct perfusion: stoke + tumour

Iodine contrast => arterial phase visualise aneurysms

A2 ME3031 NEURO (7 decks)

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