Neurocritical care focuses on critically ill patients with primary
or secondary neurological problems. Initially neurocritical care
was developed to manage postoperative neurosurgical patients;
it then expanded to the management of patients with traumatic
brain injury (TBI), intracranial hemorrhage and complications of
subarachnoid hemorrhage, including vasospasm, elevated
intracranial pressure (ICP) and the cardiopulmonary
complications of brain injury (Bamford 1992). The striking
improvements noted in many studies suggest that high-quality
neurocritical care with the delivery of targeted therapeutic
interventions does have an impact, not only on survival, but
importantly also on the quality of survival.
Types of Brain Injuries
Primary brain injuries
Ischemic brain injury: either global, which includes cardiac
arrest or anoxia, or regional ischemic brain injury, which
includes vasospasm, compression of blood vessels or stroke.
Stroke can be classified into ischemic and hemorrhagic strokes.
Ischemic stroke accounts for 80% of all strokes and can be
further classified into thrombotic or embolic stroke; ischemic
40 | Critical Care in Neurology
thrombotic stroke accounts for 77% while ischemic embolic
stroke constitutes the remainder.
Hemorrhagic strokes constitute 10-20% of all strokes, and can
be further classified into two types, the intracerebral
hemorrhage that constitutes up to 75% and the subarachnoid
hemorrhage that makes up the other 25%.
Acute ischemic stroke is the third leading cause of death in
industrialized countries and the most frequent cause of
permanent disability in adults worldwide, so understanding the
pathogenesis of ischemic stroke is mandatory. Despite great
strides in understanding the pathophysiology of cerebral
ischemia, therapeutic options remain limited. Only recombinant
tissue plasminogen activator (rTPA) for thrombolysis is
currently approved for use in the management of acute ischemic
stroke.
However, its use is limited by its short therapeutic window (3-
4.5 hours), complications from the risk of hemorrhage, and the
potential damage from reperfusion injury. Effective stroke
management requires recanalization of the occluded blood
vessels. However, reperfusion can cause neurovascular injury,
leading to cerebral edema, brain hemorrhage, and neuronal
death by apoptosis or necrosis (Hajjar 2011).
Central nervous system (CNS) infections: Acute onset fever
with altered mental status is a problem commonly encountered
by the physician in the emergency setting. “Acute febrile
encephalopathy” is a commonly used term for description of the
altered mental status that either accompanies or follows a short
febrile illness. CNS infections are the most common cause of
nontraumatic disturbed consciousness. The etiologic agents may
be viruses, bacteria, or parasites. Central nervous system
infections are classified into categories beginning with those in
immunocompetent hosts followed by infection with the human
immunodeficiency virus (HIV) and its opportunistic infections.
The viruses responsible for most cases of acute encephalitis in
immunocompetent hosts are herpes viruses, arboviruses, and
enteroviruses. Neurotropic herpes viruses that cause
Brain Injuries | 41
encephalitis predominantly in immunocompetent hosts include
herpes simplex virus 1 (HSV-1) and 2 (HSV-2), human herpes
virus 6 (HHV-6) and 7 (HHV-7), and Epstein-Barr virus (EBV).
Cytomegalovirus (CMV) and varicella-zoster virus (VZV) may in
some situations cause encephalitis in immunocompetent
patients, but more commonly they produce an opportunistic
infection in immunocompromised individuals, such as those
with HIV infection, organ transplant recipients, or other patients
using immunosuppressive drugs. HSV-1 is the most common
cause of severe sporadic viral encephalitis in the United States;
diagnosis has been become more familiar due to the availability
of cerebrospinal fluid (CSF) polymerase chain reaction (PCR)
analysis techniques that allow for rapid, specific, and sensitive
diagnoses. The use of CSF PCR instead of brain biopsy as the
diagnostic standard for HSV encephalitis has expanded
awareness of mild or atypical cases of HSV encephalitis. Adult
encephalitis is caused by 2 viral serotypes, HSV-1 and HSV-2.
Patients with greater than 100 DNA copies/μL HSV in CSF are
more likely than those with fewer copies to have a reduced level
of consciousness, more significant abnormal findings on
neuroimaging, a longer duration of illness, higher mortality, and
more sequelae (Domingues 1997). EBV is almost never cultured
from CSF during infection, and serological testing is
inconclusive, so CSF PCR diagnosis is mandatory.
Semiquantitative PCR analysis of EBV DNA suggests that copy
numbers are significantly higher in patients with active EBV
infection. HHV-6 and -7 can cause exanthema subitum, and
appear to be associated with febrile convulsions, even in the
absence of signs of exanthema subitum. Almost all children
(>90%) with exanthema subitum have HHV-6 or HHV-7 DNA in
CSF. Inflammatory primary brain damage like meningitis and
encephalitis come from pyogenic infections that reach the
intracranial structures in one of two ways - either by
hematogenous spread (infected thrombi or emboli of bacteria) or
by extension from cranial structures (ears, paranasal sinuses,
osteomyelitic foci in the skull, penetrating cranial injuries or
42 | Critical Care in Neurology
congenital sinus tracts). In a good number of cases, infection is
iatrogenic, being introduced in the course of cerebral or spinal
surgery, during the placement of a ventriculoperitoneal shunt or
rarely through a lumbar puncture needle. Nowadays, nosocomial
infections are as frequent as the non-hospital acquired variety.
The reason for altered sensorium in meningitis is postulated to
be the spillage of inflammatory cells to the adjacent brain
parenchyma and the resultant brain edema (Levin 1998).
Compressive brain injury: e.g., tumors and cerebral brain
edema are considered as important causes for impairment of the
level of consciousness. During tumor growth, cerebral tissues
adjacent to the tumor and nearby venules are compressed,
which results in elevation of capillary pressure, particularly in
the cerebral white matter, and there is a change in cerebral
blood flow and consequently intracranial pressure. At that stage
the tumor begins to displace tissue, which eventually leads to
displacement of tissue at a distance from the tumor, resulting in
false localizing signs such as transtentorial herniations,
paradoxical corticospinal signs of Kernohan and Woltman, third
and sixth nerve palsies and secondary hydrocephalus, originally
described in tumor patients.
or secondary neurological problems. Initially neurocritical care
was developed to manage postoperative neurosurgical patients;
it then expanded to the management of patients with traumatic
brain injury (TBI), intracranial hemorrhage and complications of
subarachnoid hemorrhage, including vasospasm, elevated
intracranial pressure (ICP) and the cardiopulmonary
complications of brain injury (Bamford 1992). The striking
improvements noted in many studies suggest that high-quality
neurocritical care with the delivery of targeted therapeutic
interventions does have an impact, not only on survival, but
importantly also on the quality of survival.
Types of Brain Injuries
Primary brain injuries
Ischemic brain injury: either global, which includes cardiac
arrest or anoxia, or regional ischemic brain injury, which
includes vasospasm, compression of blood vessels or stroke.
Stroke can be classified into ischemic and hemorrhagic strokes.
Ischemic stroke accounts for 80% of all strokes and can be
further classified into thrombotic or embolic stroke; ischemic
40 | Critical Care in Neurology
thrombotic stroke accounts for 77% while ischemic embolic
stroke constitutes the remainder.
Hemorrhagic strokes constitute 10-20% of all strokes, and can
be further classified into two types, the intracerebral
hemorrhage that constitutes up to 75% and the subarachnoid
hemorrhage that makes up the other 25%.
Acute ischemic stroke is the third leading cause of death in
industrialized countries and the most frequent cause of
permanent disability in adults worldwide, so understanding the
pathogenesis of ischemic stroke is mandatory. Despite great
strides in understanding the pathophysiology of cerebral
ischemia, therapeutic options remain limited. Only recombinant
tissue plasminogen activator (rTPA) for thrombolysis is
currently approved for use in the management of acute ischemic
stroke.
However, its use is limited by its short therapeutic window (3-
4.5 hours), complications from the risk of hemorrhage, and the
potential damage from reperfusion injury. Effective stroke
management requires recanalization of the occluded blood
vessels. However, reperfusion can cause neurovascular injury,
leading to cerebral edema, brain hemorrhage, and neuronal
death by apoptosis or necrosis (Hajjar 2011).
Central nervous system (CNS) infections: Acute onset fever
with altered mental status is a problem commonly encountered
by the physician in the emergency setting. “Acute febrile
encephalopathy” is a commonly used term for description of the
altered mental status that either accompanies or follows a short
febrile illness. CNS infections are the most common cause of
nontraumatic disturbed consciousness. The etiologic agents may
be viruses, bacteria, or parasites. Central nervous system
infections are classified into categories beginning with those in
immunocompetent hosts followed by infection with the human
immunodeficiency virus (HIV) and its opportunistic infections.
The viruses responsible for most cases of acute encephalitis in
immunocompetent hosts are herpes viruses, arboviruses, and
enteroviruses. Neurotropic herpes viruses that cause
Brain Injuries | 41
encephalitis predominantly in immunocompetent hosts include
herpes simplex virus 1 (HSV-1) and 2 (HSV-2), human herpes
virus 6 (HHV-6) and 7 (HHV-7), and Epstein-Barr virus (EBV).
Cytomegalovirus (CMV) and varicella-zoster virus (VZV) may in
some situations cause encephalitis in immunocompetent
patients, but more commonly they produce an opportunistic
infection in immunocompromised individuals, such as those
with HIV infection, organ transplant recipients, or other patients
using immunosuppressive drugs. HSV-1 is the most common
cause of severe sporadic viral encephalitis in the United States;
diagnosis has been become more familiar due to the availability
of cerebrospinal fluid (CSF) polymerase chain reaction (PCR)
analysis techniques that allow for rapid, specific, and sensitive
diagnoses. The use of CSF PCR instead of brain biopsy as the
diagnostic standard for HSV encephalitis has expanded
awareness of mild or atypical cases of HSV encephalitis. Adult
encephalitis is caused by 2 viral serotypes, HSV-1 and HSV-2.
Patients with greater than 100 DNA copies/μL HSV in CSF are
more likely than those with fewer copies to have a reduced level
of consciousness, more significant abnormal findings on
neuroimaging, a longer duration of illness, higher mortality, and
more sequelae (Domingues 1997). EBV is almost never cultured
from CSF during infection, and serological testing is
inconclusive, so CSF PCR diagnosis is mandatory.
Semiquantitative PCR analysis of EBV DNA suggests that copy
numbers are significantly higher in patients with active EBV
infection. HHV-6 and -7 can cause exanthema subitum, and
appear to be associated with febrile convulsions, even in the
absence of signs of exanthema subitum. Almost all children
(>90%) with exanthema subitum have HHV-6 or HHV-7 DNA in
CSF. Inflammatory primary brain damage like meningitis and
encephalitis come from pyogenic infections that reach the
intracranial structures in one of two ways - either by
hematogenous spread (infected thrombi or emboli of bacteria) or
by extension from cranial structures (ears, paranasal sinuses,
osteomyelitic foci in the skull, penetrating cranial injuries or
42 | Critical Care in Neurology
congenital sinus tracts). In a good number of cases, infection is
iatrogenic, being introduced in the course of cerebral or spinal
surgery, during the placement of a ventriculoperitoneal shunt or
rarely through a lumbar puncture needle. Nowadays, nosocomial
infections are as frequent as the non-hospital acquired variety.
The reason for altered sensorium in meningitis is postulated to
be the spillage of inflammatory cells to the adjacent brain
parenchyma and the resultant brain edema (Levin 1998).
Compressive brain injury: e.g., tumors and cerebral brain
edema are considered as important causes for impairment of the
level of consciousness. During tumor growth, cerebral tissues
adjacent to the tumor and nearby venules are compressed,
which results in elevation of capillary pressure, particularly in
the cerebral white matter, and there is a change in cerebral
blood flow and consequently intracranial pressure. At that stage
the tumor begins to displace tissue, which eventually leads to
displacement of tissue at a distance from the tumor, resulting in
false localizing signs such as transtentorial herniations,
paradoxical corticospinal signs of Kernohan and Woltman, third
and sixth nerve palsies and secondary hydrocephalus, originally
described in tumor patients.
