Decreased production
Abnormally low platelet production may be caused by:
Dehydration, Vitamin B12 or folic acid deficiency
Leukemia, myelodysplastic syndrome, or aplastic anemia
Decreased production of thrombopoietin by the liver in liver failure
Sepsis, systemic viral or bacterial infection
Leptospirosis
Hereditary syndromesACTN1-related thrombocytopenia
Amegakaryocytic thrombocytopenia with radio-ulnar synostosis
ANKRD26 related thrombocytopenia
Autosomal dominant thrombocytopenia
Bernard–Soulier syndrome (associated with giant platelet disorder)
Congenital amegakaryocytic thrombocytopenia
Congenital amegakaryocytic thrombocytopenia and radioulnar synostosis
CYCS-related thrombocytopenia
Epstein syndrome (associated with giant platelet disorder)
ETV6 related thrombocytopenia
Fanconi anemia
Filaminopathies A
FYB related thrombocytopenia
Glanzmanns thrombasthenia
GNE myopathy with congenital thrombocytopenia
Gray platelet syndrome (associated with giant platelet disorder)
Harris platelet syndrome (associated with giant platelet disorder)
Macrothrombocytopenia and hearing loss
May–Hegglin anomaly (associated with giant platelet disorder)
MYH9-related disease (associated with giant platelet disorder)
PRKACG-related thrombocytopenia
Paris-Trousseau thrombocytopenia/Jacobsen syndrome
Sebastian syndrome
SLFN14-related thrombocytopenia
Stormorken syndrome
TRPM7-related thrombocytopenia
Thrombocytopenia absent radius syndrome
Tropomyosin 4-related thrombocytopenia
TUBB1-related thrombocytopenia
Upshaw–Schulman syndrome
Wiskott–Aldrich syndrome
X-linked thrombocytopenia
X-linked thrombocytopenia with thalassemia

Increased destruction
Abnormally high rates of platelet destruction may be due to immune or nonimmune conditions, including:
Immune thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
Hemolytic–uremic syndrome
Disseminated intravascular coagulation
Paroxysmal nocturnal hemoglobinuria
Antiphospholipid syndrome
Systemic lupus erythematosus
Post-transfusion purpura
Neonatal alloimmune thrombocytopenia
Hypersplenism
Dengue fever
Gauchers disease
Zika virus

Medication-induced
These medications can induce thrombocytopenia through direct myelosuppression:
Valproic acid
Methotrexate
Carboplatin
Interferon
Isotretinoin
Panobinostat
H2 blockers and proton-pump inhibitors

Other causes
Lab error, possibly due to the anticoagulant EDTA in CBC specimen tubes; a citrated platelet count is a useful follow-up study
Snakebite
Niacin toxicity
Lyme disease
Thrombocytapheresis (also called plateletpheresis)
Niemann–Pick disease

Diagnosis
Laboratory tests for thrombocytopenia might include full blood count, liver enzymes, kidney function, vitamin B12 levels, folic acid levels, erythrocyte sedimentation rate, and peripheral blood smear.
A specific cause of the infarction should be looked for, such as diabetes, polyarteritis nodosa (inflammatory damage of vessels) or systemic lupus erythematosus. Neurosyphilis is also a known cause. Other causes include:
Treatment is supportive and aims to relieve symptoms. The prognosis is dependent upon individual circumstances and factors. Posterior spinal artery syndrome
Posterior spinal artery syndrome is much rarer than its anterior counterpart as the white matter structures that are present are much less vulnerable to ischemia since they have a better blood supply. When posterior spinal artery syndrome does occur, dorsal columns are damaged and ischemia may spread into the posterior horns. Clinically the syndrome presents as a loss of tendon reflexes and loss of joint position sense

Transient ischemic attack
Transient ischemic attacks (TIAs) rarely affect the spinal cord and usually affect the brain; however, cases have been documented in these areas. Spinal arteriovenous malformations are the main cause and are represented later in this article. However, TIAs can result from emboli in calcific aortic disease and aortic coarctation. Spinal arteriovenous malformations
Spinal arteriovenous malformations (AVMs, or angiomatous malformations) are congenital (from birth) abnormalities of blood vessels. Arteries that directly communicate with veins bypass the capillary network (which has not yet developed) and thus creates a shunt. AVMs appear as a mass of convoluted, dilated vessels. In regards to the spinal cord, they are usually located in the thoracolumbar region (between the thoracic and lumbar regions, 60% of the time), as opposed to the upper thoracic (20%) and cervical regions (approximately 15%).