Menopause Symptoms Reduced by Cold Water Swimming

 Sometimes in  dreamland of a neurologist 

How good it would have been if there existed a common unifying etiopathologic theory for  different neurological disorders.

Common involvement among them appears to be of neuroplasticity and glial cells.

How neuroplasticity ?

..Neurons discharge in synaptic cleft  >This stimulates adjacent glial (e.g.asrocyte) cell  >Glial cell response may 

be anatomical or biochemical change (syneptogenesis,synaptic modulation,synaptic extinction) with increase or 

decrease  in synthesis of neurohumoral molecules  > Networks developed or deleted  >New networks established

 as the result of deletion or formation of synapses  >These networks comprise of excitable neurons and associated 

non excitable glial cells .

Now this newly formed succeptible system will stimulate or depress or destroy neurons to cause clinical presentation of diseases like headache , epilepsy, movement disorders, neurodegeneration.

 Assumptions favoured by - 

1. Episodic nature of clinical presentations e.g. headache, seizures(threshold crossed e g .synthesis of particular molecules have gone above some level).

2. Triggers (some particular triggers can cause release of molecules  early in the susceptible network) for hedache ,for seizures and PKD.

3. Progressive nature of episodic diseases e.g.in temporal lobe epilepsy glial response to already abnormal small firing neurons may be responsible for progression of disease.Recurrence of seizures after very long time of surgery(Is nidus is left at cellular level in adjacent glial cell by induction)

 Means glia respond to neuron and other glia.

4.Valproate resistance? recently reported in some seizure patients may be due to similar chronic response of glial cells making neurons and its channels less responsive to the drug (itself the disease is progressive).

5.Possiblity of a  nidus is always there in all these , even after treatment with surgery.

  Glial cells appears to be having harbinger of slow changes that results in a conducive neurohumoral environment for neuronal excitability or disruption. Hence the clinical presentations of diseases  are episodic , trigger prone ,sometimes rhythmic with increasing intensity or relentlessly progressive  if permanent changes has occurred rather than modulation.

Modulation may be  occuring in epilepsy, headache and movement disorders whereas permanent changes in neurodegeneration.

Now come out of dreams as this  -

Needs focused work on glial cells of brain about  levels of different anatomical and biochemical changes in glia in autopsy and epilepsy surgery samples.