Where it sits in our practice
Most patients at Parklands Mindcare Centre are treated effectively with standard psychiatric care: assessment, medication, lifestyle support, and therapy referral where indicated (see services).
The ketamine programme is the specialty layer on top of that, reserved for the smaller group of patients with severe and treatment-resistant conditions where the literature, and Dr. Nabiswa's clinical experience, support a meaningful response. It is not a first-line treatment, and we do not offer it to every patient who asks for it.
In one paragraph
Ketamine acts on a different system in the brain than traditional antidepressants. At the low, monitored doses used in clinical psychiatric practice, it can produce a meaningful shift within hours and supports new neural connections that allow therapy and lifestyle change to take hold.
Mechanism
How ketamine works in the brain.
Ketamine acts by inhibiting N-methyl-D-aspartate (NMDA) receptors, which are involved in pain transmission and mood regulation. Blocking these receptors triggers a cascade of helpful changes:
- A surge in glutamate, an excitatory neurotransmitter that supports learning, memory, and mood.
- Downstream increases in serotonin and dopamine, two neurotransmitters closely tied to well-being.
- A rise in brain-derived neurotrophic factor (BDNF), a protein that supports the growth and survival of neurons.
Together, these changes drive neuroplasticity: the brain forms new synaptic connections and strengthens existing ones. This is the mechanism behind ketamine's rapid antidepressant and anxiolytic effects. Ketamine also has anti-inflammatory properties, which appear to contribute to its benefits in chronic pain syndromes such as migraine and fibromyalgia.
Comparison
Why ketamine is different from standard antidepressants.
| Aspect | Standard antidepressants | Ketamine therapy |
|---|---|---|
| Time to effect | 3 to 6 weeks | Hours to days |
| Response rate | Around 40 to 50% | Around 70 to 80% in severe cases |
| Mechanism | Serotonin or norepinephrine reuptake | NMDA receptor modulation, glutamate, BDNF, neuroplasticity |
| Anti-suicidal effect | Slow, indirect | Rapid, observed within hours in clinical practice |
Who it is for
Conditions we consider.
The programme is designed for adults with severe or treatment-resistant presentations across a defined set of neuropsychiatric conditions. Suitability is decided after a thorough psychiatric and medical assessment.
- Treatment-resistant depression (after at least two adequate antidepressant trials)
- Severe major depressive disorder, especially with significant suicidal ideation
- Bipolar depression, alongside the underlying mood-stabilising regimen
- Severe anxiety, panic disorder, and social anxiety that has not responded to standard care
- Post-traumatic stress disorder, often as an adjunct to trauma-focused therapy
- Severe, treatment-resistant obsessive-compulsive disorder
- Acute suicidal ideation in the context of severe depression
- Selected chronic pain syndromes, including migraine and fibromyalgia
Honest framing
Is ketamine a cure?
No. Ketamine is not a cure, and we will never tell you that it is. What it can do, when administered correctly to the right candidate, is provide rapid and meaningful relief that creates a window for therapy, lifestyle change, and continued psychiatric care to take hold.
Compliance language
- Ketamine is not a cure.
- Suitability is decided after a thorough assessment.
- We do not offer ketamine to every patient who asks for it.
- Ketamine is one of several treatments at Parklands Mindcare Centre, not the practice itself.
Read about how treatment works.
From assessment to monitored infusion to follow-up, the patient pathway for both standard psychiatric care and the ketamine programme.
See how it works