Research | Tardive Dyskinesia

Prognosis: "there is no known cure or treatment option to improve symptoms. In fact, many physicians will simply opt to change the patient's medications or eliminate medication use altogether although, ultimately, symptoms of tardive dyskinesia may not improve". [Source]

What Tardive Dyskinesia is:
Antispychotics cause the disorder which is mainly characterized by involuntary movements more often in the face and hands.

"They are often mistaken for psychiatric disturbances and patients may be shunned. During episodes of dystonia, opposing muscles that should relax contract. This can result in a limb that appears distorted. One of the most common manifestations is an ankle that twists and won't bear weight. In some cases, muscle groups that should be uninvolved in the activity being attempted will get involved. The result can be shoulders that swing violently during walking or an entire arm and shoulder that cramp and contort while the hand is holding a pen. In some instances, the opposing hand/arm/shoulder may also contort in a perverse sympathy." [Source]

Tardive dystonia is a syndrome of sustained muscle contractions, frequently causing either (a) twitching and repetitive movements, or (b) abnormal postures (14). Blepharospasm, grimacing, torticollis, retrocollis, and the Pisa syndrome are characteristic movements of tardive dystonia. [The Treatment of Tardive Dyskinesia] 

Antipsychotics work by blocking dopamine receptors along three pathways, and over the long-term, these pathways become increasingly dysfunctional (at least in a high percentage of patients.) The dysfunction in the basal ganglia leads to tardive dyskinesia. The dysfunction in the limbic system and the frontal lobes leads to tardive psychosis and tardive dementia.

So, the antipsychotics blocked my dopamine and as a result, I now have TOO little dopamine: 

Dopamine is defined as a catecholamine. This means that it is a hormone functioning as a neurotransmitter. The body's nervous system is a sophisticated communication network with the brain sending signals to the various systems through electrochemical impulses. These signals travel through the nerves to the terminals, where they interface with receptors on the surface of cells. In order for those signals to pass from the nerve endings, or synapses, to the cell receptors, dopamine — in very specific amounts — must be present. Dopamine also affects emotional state, perceptions, behavior and cognitive thinking. 

This paper proposes that the neuropsychiatric symptoms of tardive dyskinesia, akathisia and pseudoparkinsonian tremor are modulated by a noradrenergic pathway that projects from the locus coeruleus to the linbic system. -AND- Noradrenergic modulation of the limbic system by way of the locus coeruleus accounts for a number of clinical observations, such as the worsening of tardive dyskinesia by stress, the greater risk for tardive dyskinesia in patients with affective disorder, the time-of-onset of tardive dyskinesia, and the coexistence of tardive dyskinesia and pseudoparkinsonism. [source]

The influence of stress on dopamine receptors: 

Besides the qualitative approach to coping with stress, what bodily mechanisms are responsible for dealing with anxiety? The nervous system is almost solely credited with this task. The complex interaction system between billions of individual neurons facilitates large number of behaviors that result due to inputs originating inside and outside the organism. Spaces between neighboring neurons are called synapses, and one way in which they communicate is by sending chemical signals called neurotransmitters across the presynaptic membrane to the postsynaptic membrane. Years of nervous system research have determined that stress activates the neurotransmitter, dopamine. [source]

Although some alternatives and dopamine agonists (drugs that help to restore normal levels of dopamine) have been of some use in treating tardive dyskinesia, the best treatment found thus far is prevention. [source]

Holistic Solutions for Tardive Dyskinesia:

1.  1,600 IU of vitamin E [Source]
2. Vitamin B6 [source]
3. Ginko biloba, 240 mg/day [source]
4. Tarvil Amino Acids [source]
5. Cannabis Oil {[One Study Only for Tardive Dyskinesia] [The afore mentioned study in PubMed] [Cannabis and cannabanoids] [Dr. Sanjay Gupta and Tardive Dyskinesia on Medical Efficacy List] [Cannabis Oil, a Natural Cancer Cure, Natural News] 
1. CB₁ receptors are found primarily in the brain, to be specific in the basal ganglia and in the limbic system, including the hippocampus. [source]
2. Cannabinoid receptors are activated by three major groups ofligands, endocannabinoids (produced by the mammalian body), plant cannabinoids (such as THC, produced by the cannabis plant) and synthetic cannabinoids (suchcaas HU-210). [source]
3. The CB₁ receptor is expressed mainly in the brain (central nervous system or "CNS"), but also in the lungs, liver and kidneys. [Source]
4. U.S. National Library of Medicine's take on CBs. [source]
5. Cannabinoids and Dopamine receptors [source]
6. However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons. [source]
7. This is the ULTIMATE research that advocates for the positive use of cannabis in Tardive dyskinesia patients!