Neuro Physiology Flashcards
Autoregulation of CBF
Myogenic
Local
Neural
Costant between CPP of 60- 160 mmHg
Hyperbaric oxygen and cerebral blood flow
Although PaO2 has a far lesser effect on CBF vs PCO2
Hyperbaric oxygen can reduce cerebral blood flow by ~20%
Total volume CSF
130 -150 ml
100ml spinal cord
40ml in ventricles
Normal CSF pressure
0.5-1 kPa
Production of CSF
Choroid plexus in lateral, third and fourth ventricles
L, 3rd and 4th
~500ml / day
Foramin of Luschka
Lateral
Foramin of Magendie
Medial
Areas in which blood-brian barrier is permeable - fenestrated endothelium
Third and fourth ventricles
-Chemoreceptor trigger zone at floor of fourth ventricle
-Angiotensin II passes to the vasomotor centre in this region to increase sympathetic outflow and causes vasoconstriction of peripheral vessels
Posterior pituitary
-Allows production of ADH and oxytocin into circulation
Hypothalamus
-this allows the release of releasing or inhibitory hormones into the portal– hypophyseal tract (to anterior pituitary)
Consequences of rising ICP
Hydrocephalus
-Seen in posterior fossa lesions due to ocmpression of aqueduct
Ischaemia
-Rising ICP reduces CPP and therefore CBF
Herniation
-Compression of brain via herniation
Pupilly dilatation and raised ICP
–> oculomotor nerve compression
= Transtentorial herniation
Cortical blindess and raised ICP
= Transtentorial herniation
Resting membrane potential of axon
negative 70mV
-70mV
Depolarisation
Axon membrane potential goes form -70 –> +50mV
Absolute and relative refractory
During action potential = absolute refraction
During repolarisation = relative refraction, larger stimulus can cause another action potential
Mechanism of depolarisation and repolarisation
The Na+ channel activates much faster than the K+
channel.
This explains the rapid influx of Na+; the
channel also closes much faster; the K+ channel
remains open over a longer period than the Na+
channel and is responsible for repolarisation as K+
is released and the membrane potential falls back
to its negative value
Nodes of Ranvier
Gaps in between myelinated axons
Points of depolarisation
Increases speed of transmission as between nodes the axon depolarises quickly and entriely
= saltatory conduction
Aα axons
Motor
Propioception
Aβ axons
Touch
Pressure
Aγ axons
Muscle spindles
Aδ axons
Pain
(myelinated version of pain fibres)
C-fbres axons
Unmyelinated pain neurons
B axons
Autonomic
Breakdown of amine neurotransmitters
Monoamine oxidase: breaks down neurotransmitter taken up at PRE-synaptic neuron
Catechol-O-methyl transferase breaks down catecholamine in post-synaptic neuron
Glutamate + Aspartate
Excitatory
Glycerol
Inhibitory
Substance P
Pain transmission
Kehr’s sign
Referred pain
Left-sided diaphragmatic irritation and left shoulder tip pain
Gate control theory
Modulation of pain
Descending
Periaqueductal grey matter and raphe magnus –> releasing serotonin
Locus coeruleus –> noradrenaline
Local
Naturally occurring enkephalins and endorphins at point of tansmission synpase in spinal cord
Proteins on actin filament
Actin: double strand helix
Tropomyosin: lies in groove between double-stranded helix of actin
Troponin: regular arrangement along actin filament
-Attached ot both actin nad tropomysin
-Has binding sites for Ca2+ and is involved in the regulation of contraction.
-Troponin and tropomyosin block the myosin-binding site on actin.
Rise in calcium allows removal and binding of myosin
Proteins on mysosin
Head section has binding site for ATP
–> allows release of head from actin filament
Structure: had + long tail
Troponin
-Attached to both actin and tropomyosin
-Has binding sites for Ca2+ and is involved in the regulation of contraction.
-Troponin and tropomyosin block the myosin-binding site on actin.
Rise in calcium allows removal and binding of myosin
Tropomyosin
Tropomyosin: lies in groove between double-stranded helix of actin
Rise in calcium allows removal and binding of myosin
Type I muscle fibre
Slow / postural
Type IIa muscle fibre
Type IIa or fast oxidative fibres
e.g. calf muscles
They rely on aerobic metabolism and contain myoglobin; they have moderate resistance to fatigue
Type IIb muscle fibre
Type IIb or fast glycolytic fibres
e.g. extraocular muscle
Do not contain myoglobin and thus appear white
They contain a large amount of glycogen and rely on anaerobic metabolism.
Intrafusal muscle fibres
Respond to stretch
“stretch sensory” receptor for stretch-contraction reflex arc
Precentral gyrus
Motor cortex
Frontal lobe immediately anterior to central sulcus
Corticobulbar tracts
Motor supply to cranial nerve
Corticospinal tracts
Supply spinal motor neurons
–> voluntary movement
Four descending motor inputs from brainstem
Rubrospinal tract: red nucleus
Tectospinal tract: superior colliculus of midbrain
Vestibulospinal tract: bestibular nuclei
Reticulospinal tracts: pons and medulla
Rubrospinal tract
Descending motor input from the brainstem
- Red nucleus
-Primarily innervates distal limb muscles
Tectospinal tract
Descnding motor input from brianstem
-Superior colliculus of midbrain
-Receives inputs from the visual cortex a
-Controls reflex activity in response to visual stimuli
Vestibulospinal tract
Descending motor input form brainstem
-Vestibular nuclei
-Supplies muscles of the ipsilateral side of the body.
-Innervates muscles concerned with balance and posture in response to inputs from the vestibular apparatus
Reticulospinal tract
Desnding motor input form brainstem
-Arises from pons and medulla
-Supply muscles on the ipsilateral side of the body and are important in maintaining posture and muscle tone
Cerebellum
No descending tracts
Modulation of motor coordination directly into motor cortex in precentral gyrus
Receives information from:
-Vestibular apparatus
-Visual system
-Corticospinal tracts
-Peripheral proprioceptors
