Molecular genetic testing can be used to confirm the genetic diagnosis of Coffin–Lowry syndrome or to assess pregnancy risk in affected families.Symptoms table:

Generally symptoms listed as "rare" are common in more severe cases. Imaging studies
X-ray and neuroimaging studies may be helpful in confirming a diagnosis of Coffin–Lowry syndrome. Decreased ribosomal S6 kinase activity in cultured fibroblast or transformed lymphoblast cells from a male indicates Coffin–Lowry syndrome. Studies of enzyme activity can not be used to diagnose an affected female.Molecular genetic testing on a blood specimen or cells from a cheek swab is available to identify mutations in the RSK2 gene. This testing can be used to confirm but not rule out the diagnosis of Coffin–Lowry syndrome because not all affected individuals have a detectable mutation. Treatment
There is no cure for Coffin–Lowry syndrome. Clinical objectives are centered on symptom management. Because stimulus-induced drop attacks (SIDAs) can result in physical harm to patients with the disorder, the use of medication to prevent or reduce the number of SIDA episodes is a safety priority. Physical precautionary measures have also been used to protect patients from injury, including the use of a helmet or a wheelchair. Because sudden excitement or fright can trigger a SIDA episode it is important to minimize exposure to startling stimuli. Medications prescribed include benzodiazepines (tranquilizers used to treat anxiety), valproate (used to manage epilepsy and bipolar disorder), and selective serotonin reuptake inhibitors (SSRIs) (used to treat major depression).
There is a predominance of clonal plasma cells in the bone marrow with an abnormal immunophenotype (CD38+ CD56+ CD19−) mixed in with cells of a normal phenotype (CD38+ CD56− CD19+); in MGUS, on average more than 3% of the clonal plasma cells have the normal phenotype, whereas in multiple myeloma, less than 3% of the cells have the normal phenotype. Diagnosis
MGUS is a common, age-related medical condition characterized by an accumulation of bone marrow plasma cells derived from a single abnormal clone. Patients may be diagnosed with MGUS if they fulfill the following four criteria:
A monoclonal paraprotein band less than 30 g/L (< 3g/dL);
Plasma cells less than 10% on bone marrow examination;
No evidence of bone lesions, anemia, hypercalcemia, or chronic kidney disease related to the paraprotein, and
No evidence of another B-cell proliferative disorder. Differential diagnosis
Several other illnesses can present with a monoclonal gammopathy, and the monoclonal protein may be the first discovery before a formal diagnosis is made:

Multiple myeloma
Smouldering multiple myeloma
AIDS
Chronic lymphocytic leukemia
Non-Hodgkin lymphoma, particularly Splenic marginal zone lymphoma and Lymphoplasmocytic lymphoma
Hepatitis C
Connective tissue disease such as lupus
Immunosuppression following organ transplantation
Waldenström macroglobulinemia
Guillain–Barré syndrome
Tempi syndrome
POEMS

Management
The protein electrophoresis test should be repeated annually, and if there is any concern for a rise in the level of monoclonal protein, then prompt referral to a hematologist is required.