Low-flow infarctions, also called borderzone infarctions, are considered the result of critically reduced cerebral perfusion pressure (CPP) in far-downstream brain arteries that causes critically compromised cerebral blood flow and insufficient oxygen supply in certain vulnerable brain areas. Transhemispheric and interterritorial collateral blood flow via the anterior and posterior communicating arteries and their individual distributions must be considered with respect to the site and size of borderzone infarctions. Cardiac arrest and hypotension can also cause low-flow infarcts that are usually bilateral. Although hypoxic-ischemic cerebellar damage is often found at necropsy, clinical signs of cerebellar dysfunction are rare and are usually overshadowed by cerebral abnormalities. The general medical prognosis of patients with low-flow infarcts is poor. Deaths as a result of cardiovascular complications are frequent and account for about 10% of deaths per year. An important diagnostic improvement in identifying low-flow infarcts was the use of rCBF techniques.

Lobar intracerebral hemorrhages (ICHs) involve the white matter of the cerebral lobes, and originate at the corticosubcortical gray matter-white matter junctions. Lobar hemorrhages are distinct from other forms of ICH in their clinical presentation, causes, prognosis, and management. Lobar hemorrhage has been thought to have a better prognosis than the deep hemispheric (putaminal, thalamic) and posterior fossa hemorrhages. The case fatality rates reported have ranged between 11% and 32%, in comparison with 42% for basal ganglionic and thalamic ICH, and 43% for posterior fossa hemorrhages. The observed differences in case fatality between lobar and deep ICH probably reflect variations in hematoma size and mass effect more than their superficial versus deep location. The value of medical and surgical therapy for lobar ICH will ultimately have to be determined by clinical trials involving randomization of comparable groups of patients to one or the other type of treatment.

This chapter explores the complex relationship of stroke with the usage of abusive drugs. Opiates, amphetamines, cocaine, D-lysergic acid diethylamide (LSD), marijuana, sedatives, ethanol, tobacco and phencyclidine are investigated. Hemorrhagic stroke in heroin users may be a consequence of hepatitis with liver failure and deranged clotting or of heroin nephropathy with uremia or malignant hypertension. Amphetamine-induced cerebral vasculitis has also caused ischemic stroke. Cocaine increases the likelihood of vasospasm after aneurysm rupture. D-lysergic acid diethylamide (LSD), phencyclidine and marijuana users reports symptoms of stroke. Barbiturates, benzodiazepines, and other sedative drugs can cause cerebral infarction whereas hemorrhagic stroke has not otherwise been reported. Aneurysmal rupture occurred during orgasm following amyl nitrite inhalation. Multiple mechanisms probably explain the complex association of ethanol and stroke. Smoking is a major risk factor for coronary artery and peripheral vascular disease. Tobacco increases the risk for both ischemic and hemorrhagic stroke.