Dr. Santhrani Thaakur

Cerebral Stroke

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Stroke is defined as an abrupt and devastating illness. It is deliberated as a leading cause of adult disability (Adamson et al., 2004). Approximately 15 million people worldwide suffer from stroke each year (Mackay and Mensah, 2004). It is recognized as fourth largest cause of death ranks after cancer, heart disease and respiratory disease. The estimated costs of stroke in U.S. for 2009 is $38.6 billion with an average cost of $6,018 per person (Go et al., 2014).

Strokes are caused by a blockage (called ischaemic strokes), bleeding in the brain (called hemorrhagic strokes), a primary intercerebral hemorrhage, and subarachnoid hemorrhage. The majority of strokes are ischemic strokes, which accounts for 60-85%, caused by a transient or permanent reduction in cerebral blood flow due to occlusion of cerebral artery by an embolus. Subsequently, the ischemic area is deprived of oxygen and glucose leading to neuronal cell death in brain (Lo et al., 2003). Cell death is proportional to the brain areas affected as well as to the severity and duration of the ischemic insult (Lipton, 1999).  Ischemic stroke is predominant among stroke patients, caused by the occlusion of the cerebral artery. Cerebral ischemia is associated with multiple consequences characterized by disruption of cellular homeostasis from energy failure, excitotoxicity, oxidative stress, severe mitochondrial injury, ionic imbalance leading to cellular swelling, vascular leakage, leucocyte infiltration, inflammation and apoptosis (Lakhan et al., 2009; Nakka et al., 2008; Mehta et al., 2007). These consequences eventually contribute to neuronal cell death.

Stroke is is defined as a “brain attack” occurs when a blood clot blocks the blood flow in a vessel or artery or when a blood vessel breaks, interrupting blood flow to an area of the brain. When either of these things happens, brain cells begin to die.  When brain cells die during a stroke, abilities controlled by that area of the brain are lost. These include functions such as speech, movement and memory.  The specific abilities lost or affected depend on the location of the stroke and on its severity (i.e., the extent of brain cell death) (National Stroke Association, 2003). The World Health Organization (WHO) clinically defines stroke as “the rapid development of clinical signs and symptoms of a focal neurological disturbance lasting more than 24 hours or leading to death with no apparent cause other than vascular origin” (World Health Organization, 2005).


Episodes of stroke are reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia (Ashrafian, 2010). Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon (Thompson, 1996). The word stroke was used as a synonym for apoplectic seizure in as early as 1599 and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Wepfer (1620–1695) identified that the cause of hemorrhagic stroke is bleeding in brain (Thompson, 1996; NINDS, 1999) and the cause of ischemic stroke is blockage of cerebral arteries (NINDS, 1999). Virchow first described the mechanism of thrombo embolism as a major factor (Schiller, 1970). It was believed for many years that brain ischemia eventually leads to irreversible damage. In 1974, Hossmann and Zimmerman challenged this assumption using animal studies and demonstrated that ischemia induced in mammalian brains for up to an hour recovered partially. Accordingly, this discovery raised the possibility of intervening brain ischemia before the damage becomes irreversible (Raichle, 1983).