Insomnia pathophysiology

Since insomnia is a complex and multifaceted disorder, there is no single pathophysiologic explanation for its various manifestations. Current hypotheses focus on a combination of possible models that incorporate physiologic, cognitive, and cortical arousal. Most insomnia models focus on hyperarousal and its interference with the initiation or maintenance of sleep. 

If the balance between excitatory and inhibitory activity is shifted pharmacologically in favour of GABAergic transmission, then anxiolysis, sedation, amnesia and ataxia arise. On the other hand, an attenuation of the GABAergic system results in arousal, anxiety, restlessness, insomnia, exaggerated reactivity and even seizures. These pharmacological manifestations point to the contribution of inhibitory neurotransmission to the pathophysiology of brain disorders. A GABAergic deficit is particularly apparent in anx-... 

Primary insomnia, with underlying pathophysiology of sleep Insomnia secondary to a psychiatric disorder Insomnia secondary to a medication or drug of abuse... 

SSRIs can cause insomnia and daytime somnolence however, the symptoms seem to reflect a sleep-wake cycle disorder. It is conceivable that disruptions in the normal pattern of melatonin secretion, particularly a delay in the normal early morning fall in plasma concentrations could be involved in the pathophysiology of these symptoms. The fact that fluvoxamine is the SSRI that is most likely... 

Evidence from preclinical and clinical data suggests that GABA plays a role both in the pathophysiology of depression and bipolar disorder and in the mechanisms of action of antidepressant agents. - Low GABA concentrations and receptor activity in the brain cause depression, palpitation, insomnia, learning disorders, and memory failure. - GABA concentration in the CSF is inversely correlated with the severity of depression. ... 

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