Causes
Unlike persistent vegetative state, in which the upper portions of the brain are damaged and the lower portions are spared, locked-in syndrome is essentially the opposite, caused by damage to specific portions of the lower brain and brainstem, with no damage to the upper brain. Injuries to the pons are the most common cause of locked-in syndrome. Possible causes of locked-in syndrome include:

Poisoning cases – More frequently from a krait bite and other neurotoxic venoms, as they cannot usually cross the blood–brain barrier
Brainstem stroke
Diseases of the circulatory system
Medication overdose
Damage to nerve cells, particularly destruction of the myelin sheath, caused by disease or osmotic demyelination syndrome (formerly designated central pontine myelinolysis) secondary to excessively rapid correction of hyponatremia [>1 mEq/L/h])
A stroke or brain hemorrhage, usually of the basilar artery
Traumatic brain injury
Result from lesion of the brain-stemCurare poisoning mimics a total locked-in syndrome by causing paralysis of all voluntarily controlled skeletal muscles. The respiratory muscles are also paralyzed, but the victim can be kept alive by artificial respiration. Diagnosis
Locked-in syndrome can be difficult to diagnose. In a 2002 survey of 44 people with LIS, it took almost three months to recognize and diagnose the condition after it had begun. Locked-in syndrome may mimic loss of consciousness in patients, or, in the case that respiratory control is lost, may even resemble death.
Partial (minimal to moderate) improvement with monotherapy, augment with another of the first-line recommendations. Stage 2: Monotherapy with an alternative drug, then augmentation. Stage 3: Possible medication combinations—lithium plus Divalproex, lithium plus atypical, or Divalproex plus atypical. Stage 4: Combination of 2-3 mood stabilizers
Stage 5: Alternate monotherapy with oxcarbazepine, ziprasidone, or aripiprazole (all Level D). Stage 6: For nonresponse or intolerable side effects—clozapine for children or adolescents, or electroconvulsive therapy (ECT) for adolescents only. BPD II, manic or mixed, with psychosis
Stage 1: Same as BPD I without psychosis except for first-line treatment warrants a combination of mood stabilizer and an atypical antipsychotic. Stages 2–4: Varying combinations and augmentations. Stage 5: Alternate monotherapy (oxcarbazepine) plus an atypical antipsychotic. (Bipolar Disorder in Children and Adolescents, 2005). Prognosis
Chronic medication is often needed, with relapses of individuals reaching rates over 90% in those not following medication indications and almost to 40% in those complying with medication regimens in some studies. Compared to adults, a juvenile onset has in general a similar or worse course, although age of onset predicts the duration of the episodes more than the prognosis. A risk factor for a worse outcome is the existence of additional (comorbid) pathologies.Children with bipolar disorder are more likely to commit suicide than other children. Epidemiology
The prevalence of bipolar in youth is estimated at 2%. History
Descriptions of children with symptoms similar to contemporary concepts of mania date back to the 18th century.