Cerebral spinal fluid
Criteria for CSF abnormalities include:
Increased opening pressure (> 200mm of H2O)
Increased Leukocytes (>4/mm3)
Elevated protein (>50 mg/dL)
Decreased glucose (<60 mg/dL)

Tumor markers
These markers can be good indirect indicator of NM but most are not sensitive enough to improve cytogical diagnosis:
Carcinoembryonic antigen (CEA)
alpha-fetoprotein
beta-human chorionic gonadotropin
carbohydrate antigen19-9
creatine-kinase BB
isoenzyme
tissue polypeptide antigen
Beta-2 microglobulin
beta-glucoronidase
lactate dehydrogenase isoenzyme-5
vascular endothelial growth factor

Treatment
There is currently no cure for leptomeningeal disease as the tumor is hard to eradicate. Current treatments for leptomeningeal tumors are palliative. The goals for treatment include prolonging survival and stabilizing neurological symptoms. Radiotherapy
Radiotherapy is used mostly for focal type of NM due to the nature of damage and success rate associated with the treatment. Radiotherapy targets the tumor and destroys the collective tissues of cancerous cells. Chemotherapy
Chemotherapy is injected directly into the cerebrospinal fluid, either by lumbar puncture (“spinal tap”) or through a surgically implanted device called an Ommaya reservoir. Intrathecal Therapy is preferred since intravenous chemotherapy do not penetrate the BBB. The most common chemicals used are liposomal cytarabine (DepoCyte) and intrathecal methotrexate (MTX). The downside of a spinal tap diagnosis is that while it is highly accurate and reliable, it can also report false-negative results. Chemotherapy is delivered intrathecally as it is hard for drugs to make it into the central nervous system. Intrathecal chemotherapy can only penetrate a few millimeters. If the tumor is any thicker, radiation is given to shrink it down.The treatment is done to reduce pressure on the brain caused by any cerebrospinal fluid buildup and to reduce the number of cancer cells causing the pressure.
Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes. Another syndrome associated with cutis laxa is Lenz-Majewski syndrome which is due to a mutation in the phosphatidylserine synthase 1 (PTDSS1) gene.In contrast, acquired cutis laxa often has a triggering event such as urticaria, drugs (such as penicillin) or neoplasms. Acquired cutis laxa may also be immunologically mediated, as it can involve dermal deposit of immunoglobulins and it can occur with autoimmune diseases. Acquired cutis laxa has been associated with granular immunoglobulin A deposits as well as abundant neutrophils. One hypothesis for the cause is excessive elastase release from neutrophils and macrophages. It has also been considered that mutations in elastin (ELN) and fibulin-5 (FBLN5) genes can increase susceptibility of elastic fibres to inflammatory degradation in acquired cutis laxa.Acquired cutis laxa has also been seen in conjunction with a number of conditions including: rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and monoclonal gammopathies. It can also occur as a postinflammatory response after urticaria. Urticarial skin fibroblasts have shown a 2- to 3- fold increase in elastase activity in a patient with acquired cutis laxa. Diagnosis
Treatment
As of 2019, there is no treatment for cutis laxa. Procedures aimed at mitigating symptoms and identifying subsequent conditions are often advised. No pharmacological  agent has been able to stop the progression of the disease. However, cosmetic surgeries are potentially an option as cutis laxa does not generally involve vascular fragility. See also
Occipital horn syndrome
List of cutaneous conditions

References
Further reading
External links

Medscape entry on Cutis Laxa