Please enable JavaScript.
Coggle requires JavaScript to display documents.
Psychosis - Coggle Diagram
Psychosis
Epilepsy
All share the mechanism of neuronal hyperactivation
Hyperactivation can be local, but then spread to the rest of the brain and become global
Mechanisms and receptors/channels involved
NMDA (+), GABA (-), Ca2+ voltage gated channels, Na+ channels, AMPA
Na+ voltage gated channel
3 conformations depending on membrane potential: open, close, inactive
Drugs should target the channel in the inactive state, because this is a sign of high brain activity (the channels goes around the 3 conformations rapidly)
Phenitoil
Potentially, also other districts are targeted, causing side effects
1 more item...
Ca2+ channels
inhibited by
Ethosuximide
Valproic acid
GABA-A R
BZD: PAM
Barbituric acid: full agonist
Side effects: sedation + respiratory arrest + death (at much higher concentrations)
New generations of drugs mimicking GABA
They stimulate GABAergic transmission, even though they do not act directly on GABA
SV2A
Expressed in Glutamatergic neurons, controlling Glu release
Reduction in the release of Glu through Latveracetam
Mitochondria involvement: ROS production and activation of caspases, causing apoptosis or necrosis
Ketogenic diet targets mitochondria, especially in neurons + astrocytes (main responsible for energy production in CNS)
Balances energy production
Reduces ROS
Promotes the switch from Glu to GABA
Reduces inflammation
However, it's also associated with side effects, especially in children
CBRs are also expressed in mitochondria
Overexpression in seizures
Downregulation of CBRs used to treat seizures
Desensitization upon chronic agonist exposure (cannabinoid treatment)
Also involved in IS suppression and addiction
Drug treatment should not last long
Keto diet instead can provide long lasting benefits
Also, none of these treatments is recommended during pregnancy
Acute mania
Migraine