The remainder are secondary to a number of conditions, including:
Subarachnoid hemorrhage (10–25% of all cases of thunderclap headache)
Cerebral venous sinus thrombosis
Cervical artery dissection
Hypertensive emergency (severely raised blood pressure)
Spontaneous intracranial hypotension (unexplained low cerebrospinal fluid pressure)
Stroke (headache occurs in about 25% of strokes but usually not thunderclap character)
Retroclival hematoma (hematoma behind the clivus in the skull, usually due to physical trauma but sometimes spontaneous)
Pituitary apoplexy (infarction or hemorrhage of the pituitary gland)
Colloid cyst of the third ventricle
Meningitis, sinusitis
Reversible cerebral vasoconstriction syndrome (previously Call-Fleming syndrome, several subtypes)
Primary cough headache, primary exertional headache, and primary sexual headacheThe most important of the secondary causes are subarachnoid hemorrhage, cerebral venous sinus thrombosis, and dissection of an artery in the neck.In subarachnoid hemorrhage, there may be syncope (transient loss of consciousness), seizures, meningism (neck pain and stiffness), visual symptoms, and vomiting. 50–70% of people with subarachnoid hemorrhage have an isolated headache without decreased level of consciousness. The headache typically persists for several days.Cerebral venous sinus thrombosis, thrombosis of the veins of the brain, usually causes a headache that reflects raised intracranial pressure and is therefore made worse by anything that makes the pressure rise further, such as coughing. In 2–10% of cases, the headache is of thunderclap character.
PBC patients have AMA against pyruvate dehydrogenase complex (PDC-E2), an enzyme complex that is found in the mitochondria. Those people who are AMA negative but with disease similar to PBC have been found to have AMAs when more sensitive detection methods are employed. Other auto-antibodies may be present:Antinuclear antibody measurements are not diagnostic for PBC because they are not specific, but may have a role in prognosis. Anti-glycoprotein-210 antibodies, and to a lesser degree anti-p62 antibodies, correlate with the diseases progression toward end-stage liver failure. Anti-gp210 antibodies are found in 47% of PBC patients. Anti-centromere antibodies often correlate with developing portal hypertension. Anti-np62 and anti-sp100 are also found in association with PBC.Abdominal ultrasound, magnetic resonance cholangiopancreatography or a CT scan is usually performed to rule out blockage to the bile ducts. This may be needed if a condition causing secondary biliary cirrhosis, such as other biliary duct disease or gallstones, needs to be excluded. A liver biopsy may help, and if uncertainty remains as in some patients, an endoscopic retrograde cholangiopancreatography, an endoscopic investigation of the bile duct, may be performed.Given the high specificity of serological markers, liver biopsy is not necessary for the diagnosis of PBC; however, it is still necessary when PBC-specific antibodies are absent, or when co-existent autoimmune hepatitis or nonalcoholic steatohepatitis  is suspected. Liver biopsy can be useful to stage the disease for fibrosis and ductopenia. Finally, it may also be appropriate in the presence of other extrahepatic comorbidities.