I met with Dr Rupert McShane and a colleague from the Oxford Interventional Psychiatry Service this week for an assessment for their self pay ketamine treatment service.

As I wrote about in my previous post, this was the second part of a two stage assessment process. The first part was a ‘desk based’ review base don the background information I shared following my referral by DrG.

This second stage was a meeting over Microsoft Teams with Dr McShane, who leads the Interventional Psychiatry Service team, which specialises in Ketamine, rTMS and ECT treatment for those suffering from treatment resistant depression.

I’m pleased and relieved to report that I ‘passed’ (if that’s the right word) the assessment and have been offered Ketamine treament in line with their standard protocol.

The treatment will consist of six infusions during which I was reach a dissociated stated. The ways in which different people experience this state depend on the person and, I believe, the dose. the experience can also differ between sessions.

The assessment itself was incredibly interesting. Dr McShane asked me some questions about my depression, some life related factors and to gather what I’d describe as contextual information.

He also provided very detailed information on the potential side effects and risks associated with treatment, in addition to the experience and what to expect during and following treatment.

Much of what Dr McShane shared with me is set out in their detailed Patient Information Leaflet which I have read multiple times, but it was still helpful to hear them and to be offered the opportunity to ask questions.

Of all the potential side effects mentioned, the only one of possible concern related to tinnitus. It seems that Ketamine can worsen tinnitus in those that suffer or cause it in those that do not.

I do suffer from unilateral tinnitus in my left ear. This may be due to Meniere’s (one diagnosis I have received for the tinnitus and dizziness I suffer) or migraine variant balance disorder (a more recent diagnosis).

Although my tinnitus is annoying, it’s manageable and I can ignore it in the main. I’d prefer it if it didn’t get worse but the truth is, I won’t know whether I suffer from that side effect without starting the treatment. Moreover, I would trade worsened tinnitus in exchange for improved mental health all day long. Hopefully I won’t have to accept that trade off. We’ll see.

Returning to the assessment itself, Dr McShane was of the view that I am a good candidate (my words not his) for treatment based on my circumstances. It’s clear that his group is very research and science led, and took the time to talk me through the findings from research on mice and the effect of stress on the lateral habenula.

Good old Wikipedia described the lateral habenula as a central structure that connects forebrain regions to midbrain regions, and acts as a hub or node for the integration of emotional and sensory processing.

It is apparently involved in the regulation of neurotransmitters including dopamine and serotonin, which are associated with anxiety disorders, and avoidance behaviours.

The habenula is also involved in motivation, emption, learning and pain, meaning that it plays an important role in depression, stress, memory and addiction.

I understand there are two parts to the habenula. The lateral habenula has ‘reward-negative’ neurons which are activated by stimuli associated with unpleasant events, absence of expected reward or punishment.

It is thought that chromic stress can lead lateral habenula hyperactivity, which causes more frequent signalling of disappointment of failure. This in turn can lead to major depression.

This is a very high level and basic synopsis of what seems to be known as the habenular model of depression. The link with ketamine comes from studies conducted with mice, described in this paper.

The research was conducted by Hailan Hu, professor of brain science at Zhejiang University, and her team.

In short, the results indicated showed ketamine can block burst firing in the lateral habenula. This in turn can help explain the rapid antidepressant affect associated with the drug. More on this can be read in this article.

Returning to Dr McShane’s feedback, the background information I provided seemed to fit with the habenular model of depression. That, in turn, suggest I may see benefits from ketamine whereas others may not (there is about a 40-50% ‘success’ rate for all patients treated at Oxford).

To me, this feedback was incredibly exciting. For the first time I may have an understanding of why I feel the way I do and maybe a scientific option for improving it – rather than just trying different medications on a ‘hit and hope basis’.

I obviously can;y get my hopes up too much so as not to be disappointed to badly if it doesn’t work. As I said last time, though, I’ll be praying (metaphorically speaking) for a positive outcome.

If the treatment does not work, Dr McShane said he would have other suggestions which might help. These would include proposing the addition of Pramipexole to my antidepressant regimen.

Pramipexole is a dopamine antagonist used in the treatment of Parkinson’s disease. Research has shown it can be very effective in the treatment of treatment resistant depression.

Having a plan A and a plan B gives me optimism, in addition to the hope that raising my Vortioxetine from 10mg to 20mg will bring some relief. My fingers and toes are crossed.