W9: Cerebral Hemispheres; SC & Periphery; Motor Control; Memory & Cognition; Sleep; Sensory Systems; Neuroradiology Flashcards
Frontal Lobe landmarks
Prefrontal Cortex
(4) Precentral Gyrus (Motor)
(44) (45) Broca’s Area
> BROCA’S APHASIA: missing small words
Parietal Lobe Landmarks
(3) (1) Postcentral gyrus (sensory)
(2)
- sup. parietal lobule: awareness of L 1/2 of body
- inf. lobule: global sensory area
> hemisensory neglect
Temporal Lobe Landmarks
(41) (42) Superior Temporal Gyrus: 1º Auditory Cortex
Wernicke’s Area (post) - dominant hemisphere
> WERNICKE’S APHASIA: fluent but meaningless
Occipital Lobe Landmarks
(17) 1º Visual cortex either side of calcacrine sulcus
(18) (19) visual assoc. areas: interpretation
Limbic Landmarks
Cingulate Hippocampus Parahippocampal Gyrus Amygdala => Memory formation + emotion
Describe the main fibre systems of the forebrain
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)
Name the components of the basal ganglia and their function
CAUDATE NUCLEUS
LENTIFORM NUCLEUS
SUBSTANTIA NIGRA
=> control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, & emotion.
Arrangement of spinal tracts at the spinal cord
DORSAL COLUMN
CORTICOSPINAL
LATERAL SPINOTHALAMIC
DORSAL COLUMN
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)
CORTICOSPINAL TRACT
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
LATERAL SPINOTHALAMIC TRACT
Ascending sensory: pain + temperature
- 1n GM /medulla synapse and exit at same level @ SC
- 2n crosses to lateral column and travels up.
Name the components of a reflex arc.
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
Muscle tone lesions
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
Brown Sequard Syndrome
Herniated C3
>ipsilateral deficit
at level of lesion: LMN lesion symptoms
below level: UMN lesion symptoms
Explain what is meant by ‘readiness potential’
measure of activity in the motor cortex and supplementary motor area of the brain leading up to voluntary muscle movement. Pre-motor planning.
Name two disorders which may occur when the basal ganglia are damaged and the sites of damage
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
Outline the essential processes involved in motor learning
Motor learning occus in the cerebellum.
List the symptoms which may be seen in patients with cerebellar disorders.
Disorder of coordination
Ataxia (which alcohol can depress further)
Outline the role of the Limbic System in learning and memory
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
Outline the differences between short term memory and long term memory
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
Amnesias and how
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
Papez Circuit
- 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
Associations & Pathologies of Memory
• 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.
Origin of sleep & molecules & regulation
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
Explain the significance of the amplitude and frequency of EEG waves in terms of cortical activity
⇧Frequency w/ NEURONAL EXCITATION
Amplitude informs the strength of the pattern.
⇧Frequency = ⇩Amplitude Relationship
4 Main EEG Types
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
Describe the typical pattern of a night’s sleep in an adult
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
Features of REM Sleep
⇧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
Sleep Disorders
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
Explain the concept of sensory transduction
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
Lesions of 1º afferent fibres
Aalpha & AB = ipsilateral loss of touch pressure and vibration
Aδ+C = contralateral loss of nociception and temperature
(think left C3 - brown sequard)
Explain how tissue damage can lead to pain
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
Explain why pain originating from the viscera can often result in sensation being referred to a somatic structure from the same dermatomes
convergence: 2 neurones > main dermatome neurone
* referred pain from visceral > somatic structures of same dermatome *
Explain the mechanism of action of commonly used analgesic drugs.
- NSAIDS: sensitisation of prostaglandins inhibiting cyclo-oxygenase -| arachidonic acid -> prostaglandins
↓5htR sensitisation = ↓AP - 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
MRI phases
T1-weighted
- dark CSF + water
- bright fat
T2-weighted
- white CSF + water => oedema
- fat is dark
CT in Neuroradiology
Ct perfusion: stoke + tumour
Iodine contrast => arterial phase visualise aneurysms
