Neuro physiology Flashcards
what neurotransmitters do the PNS and SNS use
at both presynaptic to postsynaptic and postsynpatic to effector - the PNS uses ACh
at presynaptic to post SNS uses ACh, at post to effector SNS uses NE, Pre to the adrenal medulla uses ACh - which then has hormonal response.
where do we find the lateral horn of the spinal cord
T1-L2 just where we find the paravertebral sympathetic chain ganglion
what cranial nerves does the PNS have effect on
oculomotor, glossopharyngeal, vagus
which nerve does most of the PNS function in the body
the vagus nerve carries out around 85% of the parasympathetic function in the body, providing the PNS innervation to the heart, lungs and GIT
whats the types of seizures
focal onset - confined area but can then spread. can have motor onset or non-motor onset
or generalised onset. can also have motor or non motor onset. these are the stereotypical seizures that people think of
whats the name of the stereotypical seizure that we think of
tonic clonic seizures
whats a motor vs non motor seizure
These involve abnormal movements due to excessive electrical activity in the brain.
These seizures do not primarily involve movement but rather affect consciousness, emotions, or sensations.
what are causes of neuronal hyperactivity in seizures
Increased synaptic transmission, reduced synaptic inhibition, increased intrinsic excitability, some combo.
whats the corticobulbar tract
neurons going from the motor cortex to the brainstem nuclei where they would then provide motor innervation for the cranial nerves
What is the role of basal ganglia and cerebellum in motor actions
Basal ganglia informs movement, sensory information about the movement via the thalamus. The basal ganglia “set the scene for how the movement wants to be done.” Cerebellum will modulate the activity that is happening, it coordinates the movements that the cortex is putting out in a way.
whats the table for the LMN lesion
power - down
tendon reflex - down
muscle tone - down
muscle atrophy - down big
plantar response - normal
why is the tendon reflex down in LMN lesions
because the lower motor neurons that are taking part in the reflex are damaged so that means the reflex cannot happen
why are muscle tone and muscle bulk down in LMN lesions
muscle bulk because the LMN is no longer innervating the muscle and with lack of nerve innervation we get a lack of muscle stimulation so it begins to atrophy
muscle tone is due to the structure of muscle and tissue properties and tonic activity of the nerve. so damage to the nerve will lower this muscle tone
why do we have gamma motor neurons in the reflex arc
Function of Gamma Motor Neurons in the Reflex Arc
Gamma motor neurons innervate intrafusal muscle fibers within the muscle spindle, which is the sensory receptor for stretch. Their role includes:
Regulating Muscle Spindle Sensitivity
When a muscle contracts, the muscle spindle could become slack and unresponsive to further stretch.
Gamma motor neurons tighten intrafusal fibers, keeping them sensitive to stretch even during contraction.
describe the withdrawal reflex when we stand on sharp things for example
on the side of the stimulus the flexors will activate to make us disengage from the painful stimuli. when the stimulus for contraction travels to the LMN it will also synapse on extensor neurons on the other side (possibly via an interneuron) to make them extend putting more weight on the other foot as the person takes their foot off of the painful stimuli.
whats the rubrospinal tract
this is from the red nucleus. this is where cell bodies in the red nucleus has outputs down the spinal cord hence rubrospinal. this pathway is important for interjoint coordination.
whats the tectospinal pathway
the start is the superior colliculus which has inputs from moving objects in the visual field. the neurons then descend down to motor neurons so that people can have motor action in response to the visual stimuli
glen Phillips has a huge one. people from asian sub-continent do not
whats the table for upper motor lesions
power down
tendon reflex up
muscle tone up
muscle atrophy mild
plantar response shows positive bubinski.
why does the tendon reflex increase and muscle tone increase
Tendon reflexes are increased as there is no longer descending motor commands to depress the strength of the reflex. So when we invoke it, it is much stronger.
Tone increases as there is again no inhibition on the reflex arc.
as the constant tone of the muscle reflex arc is what gives muscle resting tone along with other things
we get the table when we have the UMN issues, if the lesion is in the cortex, brainstem or spinal cord what can we get
if its in the cortex we can get picture, language, perceptual or frontal emotional abnormalities
brainstem may cause cranial nerve defects ontop of everything else
spinal cord injury would have possible sensory effects plus focal damage to the LMN
how does the basal ganglia feedback on cerebral cortex outputs
Dopamine aids the function of the striatum. The dopamine comes from the substantia nigra.
The cerebral cortex inputs into the striatum, in an excitatory fashion. When cortex wants to do something. Striatum then inhibits the internal globus pallidus. Then the internal globus pallidus inhibits the thalamus. And then the thalamus will feedback and excite the cortex to engage the movement.
That is all the direct pathway
Internal globus pallidus being turned off by the striatum means the thalamus is less turned off by the pallidus, which means more excitation to the cortex. So the direct pathway is a kind of go signalling pathway.
how does the indirect pathway work for cortex outputs
Sees cortex to striatum -> which inhibits the external globus pallidus, which then inhibits the subthalamic nucleus which stimulates the internal globus pallidus. And then the rest of the direct pathway happpens from there.
The indirect pathway results in turning the internal globus pallidus more, which then inhibits the thalamus more, so the thalamus is less able to excite the cortex. Which results in less strong signal or action from the cortex.
Dopamine allows this all to happen - substania nigra in the midbrain is the source.
what is the cause of parkinsons
we dont know the cause per say but the reason it happens is that we lose dopamine production by the substantial nigra
why does the lack of dopamine cause disability of parkinsons
dopamine is needed for functioning of the basal ganglia and their go and don’t go pathways. without the dopamine they both function at an equal level of activity. thus we get equal level of activity from agonists and antagonists hence the rigidity and things
symptoms of parkinsons disease
rigidity, akinesia, bradykinesia, mask face, micrographia, shuffling gait, postural instability
whats going wrong in huntingtons
there is damage to the spiny neurons in the striatum due to the excess CAG triplets in the Huntington gene
this leads to a loss of the indirect pathway leading to excess activation causing symptoms
symptoms of huntingtons
chorea - excessive random spontaneous movements. loss of voluntary movement, dementia, agitation, mania.
what are signs of cerebellar dysfunction
ataxia, intention tremour - tremour during movement, dysmetria - poor in distance judgement. n
nystagmus - rhythmic involuntary eye movements
titubation
DANISH
whats the pneumonic for remembering cerebellar dysfunction
DANISH
dysmetria, ataxia, nystagmus, intention tremour, Slurred speechm, Hypotonia
