sinus tachycardia
Orthostatic hypotension
Hypotension
Swollen tongue
Dysphagia (difficulty swallowing)
Glossodynia
Oral paraesthesiaRare (0.01-0.1% incidence) adverse effects include:

Neuroleptic malignant syndrome (Combination of fever, muscle stiffness, faster breathing, sweating, reduced consciousness, and sudden change in blood pressure and heart rate)
Tardive dyskinesia
Speech disturbance
Rhabdomyolysis
Angioedema
Blood dyscrasias such as agranulocytosis, leukopenia and neutropenia
Accommodation disorder
Pulmonary embolism
Gynaecomastia
GalactorrhoeaUnknown incidence adverse effects

Allergic reaction
Restless legs syndrome
Nausea
Oral mucosal lesions (ulcerations, blistering and inflammation)
Salivary hypersecretion
HyperprolactinaemiaAsenapine seems to have a relatively low weight gain liability for an atypical antipsychotic (which are notorious for their metabolic side effects) and a 2013 meta-analysis found significantly less weight gain (SMD [standard mean difference in weight gained in those on placebo vs. active drug]: 0.23; 95% CI: 0.07-0.39) than, paliperidone (SMD: 0.38; 95% CI: 0.27-0.48), risperidone (SMD: 0.42; 95% CI: 0.33-0.50), quetiapine (SMD: 0.43; 95% CI: 0.34-0.53), sertindole (SMD: 0.53; 95% CI: 0.38-0.68), chlorpromazine (SMD: 0.55; 95% CI: 0.34-0.76), iloperidone (SMD: 0.62; 95% CI: 0.49-0.74), clozapine (SMD: 0.65; 95% CI: 0.31-0.99), zotepine (SMD: 0.71; 95% CI: 0.47-0.96) and olanzapine (SMD: 0.74; 95% CI: 0.67-0.81) and approximately (that is, no statistically significant difference at the p=0.05 level) as much as weight gain as aripiprazole (SMD: 0.17; 95% CI: 0.05-0.28), lurasidone (SMD: 0.10; 95% CI: –0.02-0.21), amisulpride (SMD: 0.20; 95% CI: 0.05-0.35), haloperidol (SMD: 0.09; 95% CI: 0.00-0.17) and ziprasidone (SMD: 0.10; 95% CI: –0.02-0.22). Its potential for elevating plasma prolactin levels seems relatively limited too according to this meta-analysis.
Genetics
Neu-Laxova syndrome is a heterogeneous metabolic disorder caused by homozygous or compound heterozygous mutations in one of three genes: PHGDH, PSAT1 and PSPH These genes are involved in the serine biosynthesis pathway and are essential for cell proliferation. Mutations in all three genes had been previously identified as the cause of serine-deficiency syndromes. Although there is some clinical overlap between NLS and these neurometabolic disorders, the phenotype in other serine-deficiency disorders is milder. Diagnosis
The diagnosis is usually based on clinical features present at birth. Ultrasound in the second trimester may show abnormalities associates with NLS, including polyhydramnios, intrauterine growth restriction, microcephaly, proptosis and decreased fetal motility. Treatment
Serine and glycine supplementation has shown tentative benefits in those with related serine biosynthesis defects and milder forms of NLS. Prognosis
The prognosis is poor; affected individuals are either stillborn or die shortly after birth. The longest survival reported in literature is of 134 days. This syndrome is transmitted as an autosomal recessive disorder and there is a risk for recurrence of 25% in future pregnancies. References


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