The first English-language paper on the subject was published in 1947 by William Henry Mathews, describing the Tuya Butte field in northwest British Columbia, Canada. The eruptive process that builds these structures, originally inferred in the paper, begins with volcanic growth below the glacier. At first the eruptions resemble those that occur in the deep sea, forming piles of pillow lava at the base of the volcanic structure. Some of the lava shatters when it comes in contact with the cold ice, forming a glassy breccia called hyaloclastite. After a while the ice finally melts into a lake, and the more explosive eruptions of Surtseyan activity begins, building up flanks made up of mostly hyaloclastite. Eventually the lake boils off from continued volcanism, and the lava flows become more effusive and thicken as the lava cools much more slowly, often forming columnar jointing. Well-preserved tuyas show all of these stages, for example Hjorleifshofdi in Iceland.Products of volcano-ice interactions stand as various structures, whose shape is dependent on complex eruptive and environmental interactions. Glacial volcanism is a good indicator of past ice distribution, making it an important climatic marker. Since they are embedded in ice, as glacial ice retreats worldwide there are concerns that tuyas and other structures may destabilize, resulting in mass landslides. Evidence of volcanic-glacial interactions are evident in Iceland and parts of British Columbia, and it is even possible that they play a role in deglaciation.
voltage-gated calcium channel, voltage-gated potassium channel, or other currently recognized paraneoplastic antibodies) to support another diagnosis
In imaging studies no evidence for vascular, neoplastic or structural lesions that might explain the symptoms
Complete or nearly complete remission after initiation of glucocorticoid therapy. Definition
A relapsing encephalopathy occurs in association with autoimmune (Hashimotos or Ords thyroiditis), with high titers of antithyroid antibodies. Clinically, the condition may present one or more symptoms. Onset is often gradual and may go unnoticed by the patient and close associates to the patients. Symptoms sometimes resolve themselves within days to weeks, leaving a patient undiagnosed. For many other patients, the condition may result in ongoing problems with a variety of manifestations, often confusing clinicians due to the diffuse nature of symptoms. Differential diagnosis
Alzheimers disease
Cerebrovascular accidents (stroke)
Creutzfeldt–Jakob disease
Epilepsy
Migraine (including basilar, hemiplegic, and retinal types)
Other forms of autoimmune encephalitis, including forms of limbic encephalitis such as anti-NMDA receptor encephalitis
Schizophrenia
Spontaneous cerebrospinal fluid leak
Viral encephalitis
Transient ischemic attack

Treatment
Because most patients respond to corticosteroids or immunosuppressant treatment, this condition is now also referred to as steroid-responsive encephalopathy.Initial treatment is usually with oral prednisone (50–150 mg/day) or high-dose intravenous methylprednisolone (1 g/day) for 3–7 days. Thyroid hormone treatment is also included if required.Failure of some patients to respond to this first-line treatment has produced a variety of alternative treatments, including azathioprine, cyclophosphamide, chloroquine, methotrexate, periodic intravenous immunoglobulin, and plasma exchange. No controlled trials have been conducted, so the optimal treatment is not known.Seizures, if present, are controlled with typical antiepileptic agents. Prognosis
Duration of treatment is usually between 2 and 25 years.