Ok.My latest fad.
Vascular grooves.No I ‘m not talking about Dracula’s record collection.Attended meeting about microvascular decompression and have decided it is the missing explanation for everything.
The clue has been there in the form of trigeminal neuralgia all along.A perfectly obvious paroxysmal lancinating pain when classical and associated in no small part with the presence of an indenting groove in the trigeminal nerve due to apposition of a loop of superior cerebellar artery in most cases similar to facial hemispasm’s association with vessel pressure on the nerve.
NO scar tissue.just physiological pressure resulting in episodic pain.
episodes symptomatically associated with local stimulation and hence possibly alterations in blood flow+/or neural firing presumably causing dynamic alterations in vessel/nerve size and degree of contact.
point is contact causes cross firing,enhanced activation.
extrapolate to microscopic vessels in parenchyma and and you have almost limitless opportunities for cross firing and local enhancement of function which might actually be the physiological basis for non local cognitive function.
because the smallest vessels and nerve axons are arguably most intricately related in the more superficial “higher centres” of the brain that require multiple afferent and efferent coordination.
the same phenomenon on larger vessels at ,say the skull base,become manifest as more obviously pathological phenomenon.
And the regular pulsation of the brain could be a mode of transmitting the transmural vascular pressure changes to the neuronal tissue to maintain those essential cross links.
Maybe thats why non pulsatile flow in cardiac bypass results in post op cognitive defects.
And why any intracranial mass and most of all intraventricular haemorrhages have such far reaching effects on the critical global plasticity and network formation of the brain required for higher functions even though the exact locality of such masses rarely explains the global consequences on their cognition and why subsequent recovery may depend so much on the ability of collaterals to form a new global network of neurovascular coupling.
and since the facial muscles have such a high density of acetylcholine receptors and which is why suxamthonium appears to have a such marked effect on them and further more maybe also why patients recovering from a stroke have such a high frequency of what look like myoclonic facial jerks due to the higher centres trying to reactivate in the presence of dysfunctional efferents.
The tendency for seizures in an area of ischaemic damage is just revealing the hyper excitability of the nerves attempting to repair themselves and overfiring _ but maybe that firing is necessary to reestablish new networks and we are suppressing that healing process by inappropriately sedating them or treating them as seizures with anticonvulsants.
So seizures are a poor prognostic sign because they indicate the size of damage sufficient to be causing hyper excitable firing BUT the firing is not deleterious per se which may be why there is no evidence that treating them actually improves outcomes.in fact the theory that they place a strain on oxygen demand might again prove that they are trying to re-perfuse new vascular networks to try and replace the damaged ones.
hence there is no evidence that treating partial seizures is beneficial in terms of function and prognosis.
Generalised tonic clonic status epilepticus is obviously different as it is clearly a global over firing which suggests that there is such diffuse damage that there si diffuse excitability which probably is counterproductive to oxygen supply and demand balance.
and why melatonin must be better than temazepam but you cannot expect a physiological hormone to work in isolation without the other physiological cues of light and darkness.It takes teamwork after all doesn’t it Mr Gawande?
Eye patches and ear plugs are the way to go!
Tell that to the economists,Mr Soros