1. Imaging of suspected SAH:
-If its fresh, CT without contrast
-If it's older (a few days), MRI- T2* or susceptibility weighted imaging is the most sensitive for blood; alternatively you can look for cortical surface edema on T2 FLAIR as a proxy for irritation from residual or past subarachnoid blood.
2. LP & SAH:
-LPs done in an ER setting are not-infrequently traumatic, and so the presence of blood therein may not be diagnostic.
-Xanthochromia testing on the LP sample to look for blood breakdown products may be helpful
3. Hypodensity on non-contrast CT scan: infarct 
-Generally non-expansile (vs edema)
-Within the first 4-6 hours of an infarction, a noncontrast CT is likely to show nothing.
-At approx 4-8 hours, you will start to see a developing hypodensity without significant edema; it will look very hypodense at this stage, almost black.
-At around 48-72 hours is the peak of edema, and you will see hypodensity with expansile effects on nearby ventricles/sulci. This is helpful for deciding management-- i.e. if you already see a midline shift within the first 24 hours, you know it will get worse, and you are more likely to put in an EVD.
-An old infarct will look hypodense on CT, but more greyish than black, and less homogenous. You may also see hydrocephalus ex-vacuo, where the loss of local brain tissue will lead to the enlargement of nearby ventricles.
4. Other causes of hypodensity on non-contrast CT scan
-Edema: Generally expansile- look at nearby ventricles/sulci to see effacement.
-Fluid collection (i.e. cyst or abscess): look for cystic-appearing shape, etc.
5. Hyperdensity on CT scan: calcifications {DIR} Age-related physiologic and neurodegenerative calcifications: 

"Intracranial physiologic calcifications are unaccompanied by any evidence of disease and have no demonstrable pathological cause. The most common sites include the pineal gland, habenula, choroid plexus, basal ganglia, falx, tentorium, petroclinoid ligaments and sagittal sinus. Calcification of the pineal gland is seen in two-thirds of the adult population and increases with age. Pineal calcification over 1 cm in diameter or under 9 years of age may be suggestive of a neoplasm. Habenula has a central role in the regulation of the limbic system and is often calcified with a curvilinear pattern a few millimeters anterior to the pineal body in 15% of the adult population. Choroid plexus calcification is very common finding, usually in the atrial portions of the lateral ventricles (Fig. 1). Calcification in the third or fourth ventricle or in patients less than 9 years of age is uncommon. Basal ganglia calcifications are usually idiopathic incidental findings that have a 0.3–1.5% incidence and increases with age. They usually demonstrate a faint punctuate or a coarse conglomerated symmetrical calcification pattern (1) (Fig. 2). Calcifications of the falx, dura mater or tentorium cerebelli occur in about 10% of elderly population"
6. Hyperdensity on CT scan: calcifications {DIR} congenital 

"This condition is frequently seen in Sturge-Weber syndrome (SWS), tuberous sclerosis (TS) and intracranial lipoma, but rarely in neurofibromatosis (NF), Cockayne (CS) and Gorlin syndromes (GS)."
7. Hyperdensity on CT scan: calcifications {DIR} infectious 

TORCH infections, viral encephalitis, intracranial TB or fungal infection
8. Hyperdensity on CT scan: calcifications {DIR} metabolic 

"Fahr disease is a rare degenerative neurological disorder characterized by extensive bilateral basal ganglia calcifications that can lead to progressive dystonia, parkinsonism and neuropsychiatric manifestations. It is associated with defective iron transport resulting in tissue damage with extensive calcification." 

Others: parathyroid disease
9. Hyperdensity on CT scan: calcifications {DIR} vascular 

"Calcification of the intracranial arteries associated with primary atherosclerosis is more frequent in elderly people. The highest prevalence of intracranial artery calcification is seen in the internal carotid artery (60%), followed by the vertebral artery (20%), middle cerebral artery (5%), and basilar artery (5%) (13) (Fig. 15).

Other causes of vascular calcifications include aneurysm, arteriovenous malformation (AVM) and cavernous malformation. Although patent aneurysms may contain mural calcification, partially or completely thrombosed aneurysms commonly have calcifications (14) (Fig. 16). AVMs may contain dystrophic calcifications along the serpentine vessels and within the adjacent parenchyma with a prevalence of 25–30% (13) (Fig. 17). Cavernous malformation is a benign vascular hamartoma that is frequently calcified in a ’’popcorn-ball’’ fashion (15) (Fig. 18)."
10. Hyperdensity on CT scan: calcifications {DIR} neoplastic 

"The most common intracranial neoplasms associated with calcifications (16) are oligodendroglioma (70–90%), craniopharyngioma (50–80%), germ cell neoplasms (dysgerminoma, seminoma, teratoma, choriocarcinoma; 60–80%), pineal neoplasms (pineoblastoma, pineocytoma; 60–80%), central neurocytoma (50–70%), primitive neuroectodermal tumor (PNET) (50–70%), ependymoma (50%), ganglioglioma (35–50%) (Fig. 19), dysembriyonic neuroectodermal tumor (DNET) (20–36%), meningioma (20–25%), choroid plexus papilloma (25%), medulloblastoma (20%), low grade astrocytoma (20%), and pilocytic astrocytoma (10%). Calcifications are rarely seen in schwannomas, and dermoid and epidermoid tumors."