Pharmacotherapy Of Depression In Epilepsy

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Before addressing the specific treatment strategies, it is important to review these basic principles:

(i) Did the symptoms of depression appear following the introduction or increase in the dose of an AED known to cause psychiatric adverse events?

(ii) Did the psychiatric symptoms follow the discontinuation of an AED with mood-stabilizing properties (i.e. carbamazepine, oxcarbazepine, valproic acid and lamotrigine)? In such cases, the psychiatric symptoms may be the expression of recurrence of a latent psychiatric disorder that had been in remission (or masked) by the discontinued AED.

(iii) Did the psychiatric symptoms occur after the introduction of an enzyme-inducing AED (carbamazepine, phenytoin, phenobarbital, primidone, high-dose topiramate or oxcarbazepine) in a patient who was already taking a psychotropic drug for a previously recognized depression or anxiety disorder? In such a case, the symptom recurrence may have resulted from a pharmacokinetic interaction between the AED and the psychotropic drug on board that caused a drop in the psychotropic drug's serum concentration. Accordingly, a readjustment in the dose of the psychotropic drug may be sufficient to induce symptom remission.

(iv) Are the psychiatric symptoms temporally related to the seizure occurrence; that is, do they precede (pre-ictal), follow (post-ictal), both, are they the expression of an ictal event, or do they occur interictally with a peri-ictal exacerbation in severity? In the case of pre- or post-ictal without interictal symptoms, pharmacotherapy may fail to yield any benefit. Post-ictal breakthrough symptoms may occur in patients whose interictal symptoms remitted with pharmacotherapy.

(v) Is there a risk factor, other than epilepsy, for the development of the psychiatric disorder, particularly a family history in a first-degree relative?

(vi) Are the psychiatric symptoms related to the remission of seizures following a period of persistent seizures or are they associated with worsening of the patient's seizure disorder? In the former case, the symptoms may be the expression of the phenomenon known as 'forced normalization' or 'alternative psychopathology'.

Today, anti-depressant drugs of the families of the SSRIs and of the selective norepinephrine reuptake inhibitors (SNRIs) have become the first line of pharmacotherapy for primary major, dysthymic and minor depressive disorders. Fortunately, these drugs

Treatment of common co-morbid psychiatric disorders in epilepsy Table 15.2 Efficacy of SSRIs and SNRIs in primary depression and anxiety disorders

Anti-depressant drug

Depression

Panic disorder

Generalized anxiety

starting dose

(mg)

Paroxetine*

+

+

+

10

60

Sertraline*

+

+

25

200

Fluoxetine*

+

+

10

80

Citalopram*

+

10

60

Escitalopram*

+

+

+

5

30

Venlafaxinet

+

+

+

37.5

300

^Selective serotonin reuptake inhibitor (SSRI); Selective norepinephrine reuptake inhibitor (SNRI). The SSRI fluvoxamine and the SNRIs mirtazapine and duloxetine were not included in this table due to the absence of any data in patients with epilepsy.

have also been shown to have a therapeutic effect in the treatment of generalized anxiety and panic disorders, which, as stated above, are very frequent co-morbid conditions of mood disorders. Table 15.2 shows the anti-depressant drugs with anti-depressant and anxiolytic and anti-panic properties.

We must keep in mind, however, that the data available for the management of mood disorders in PWE are derived from open trials, based on the experience obtained in the treatment of primary depression disorders. Indeed, to date there has been only one controlled study published in the literature that compared under blind conditions the efficacy of two anti-depressant drugs (amitriptyline and mianserin) with placebo in major depression of PWE [16].

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