This gives information about hypertension or intracranial hypertension

1. Intracranial hypertension
Dr. Anara Kanatova

2. • Intracranial hypertension is a spectrum of
neurological disorders where cerebrospinal
fluid (CSF) pressure within the skull is elevated.
Normal CSF pressure varies by age. In general,
CSF pressure above 250 mm H20 in adults and
above 200 mm H2O in children signifies
increased intracranial pressure (ICP). It may be
idiopathic or arise as a result of neurologic
insult or injury.

3. • The human skull is a relatively fixed volume
structure of approximately 1400 to 1700 mL.
Physiologically its components consist of 80%
brain parenchyma, 10% cerebrospinal fluid, and
10% blood. Since the skull is considered an
unchangeable volume, any increase in the
volume of components within the skull or an
addition of a pathologic element will result in
increased pressure within the skull. Pathologic
structures that can cause increased ICP may
include mass lesions, abscesses, and hematomas

4. Etiology
• The physiologic volume of the brain parenchyma is a
relatively constant value in adults: however, it may be
adjusted by mass lesions or in the setting of cerebral edema.
Cerebral edema can occur with acute hypoxic
encephalopathy, large cerebral infarction, and severe
traumatic brain injury. CSF and blood volume in the
intracranial space will vary regularly as these are the primary
regulators of intracranial pressure. CSF volume is primarily
regulated via choroid plexus production at a rate of
approximately 20 mL per hour physiologically and through
its reabsorption at a similar rate by arachnoid granulations
that drain into the venous system of the skull. The control
mechanisms for maintaining appropriate CSF pressures may
become damaged in neurological injuries such as stroke or
trauma. Increased CSF production above the rate at which it
can be reabsorbed, such as a choroid plexus papilloma, leads
to increased pressure.

5. • A failure to reabsorb at a sufficient rate to match
normal secretion rate is another possibility and is seen
with arachnoid granulation adhesions after bacterial
meningitis. Ventricular obstruction may also induce
decreased reabsorption of CSF causing hydrocephalus.
The primary regulator of blood volume is via cerebral
blood flow. Diseases that obstruct venous outflows
such as venous sinus thrombosis, jugular vein
compression, or structural changes due to neck surgery
may cause blood congestion within the skull, thus
increasing pressure. Idiopathic intracranial
hypertension, also known as pseudotumor cerebri, is a
term for increased intracranial pressure due to
unknown causes with no known structural change.

6. The etiology of intracranial hypertension
can be divided into two categories:
• Primary or Intracranial Causes
• Trauma (epidural hematoma, subdural hematoma,
intracerebral hemorrhage or contusions)
• Brain tumors
• Stroke
• Nontraumatic intracerebral hemorrhage (aneurysm
rupture)
• Idiopathic or benign intracranial hypertension
• Hydrocephalus
• Meningitis

7. • Secondary or Extracranial Causes
• Hypoventilation (hypoxia or hypercarbia)
• Hypertension
• Airway obstruction
• Metabolic (drug-induced)
• Seizures
• Hyperpyrexia
• High altitude cerebral edema

8. Epidemiology
• The exact epidemiology of intracranial
hypertension depends on its etiology. However,
of special note is idiopathic intracranial
hypertension where up to 90% of affected
individuals are women of childbearing age.
Individuals with chronic hypertension or obesity
are also at an increased risk for developing
intracranial hypertension. A frequency of
occurrence has been established to be 1.0 per
100,000 in the general population, 1.6 to 3.5 per
100,000 in women, and 7.9 to 20 per 100,000 in
women who are overweight.

9. Pathophysiology
• Anytime there is an elevation in ICP, there is the risk of
subsequent injury from direct brainstem compression or
from a reduction in cerebral blood flow. Clinically, cerebral
blood flow is evaluated via measurement of cerebral
perfusion pressure where:
• Cerebral perfusion pressure = Mean arterial pressure -
Intracranial pressure
• Cerebral perfusion pressure in simpler terms is the pressure
of blood flowing to the brain and is the driving force for the
delivery of oxygen necessary for neuronal functioning.
Normally, this is a constant value of 50 to 100 mm Hg due to
autoregulation. The impact that cerebral perfusion pressure
holds is in the concept that blood flow will occur from an
area of higher concentration to an area of lower
concentration.

10. • When ICP becomes elevated, cerebral perfusion
pressures decrease, and the net driving force of blood
flow to the brain becomes decreased. The physiologic
autoregulatory response to a decrease in cerebral
perfusion pressure is to increase mean arterial
pressures systemically and to vasodilate cerebral blood
vessels. This results in increased cerebral blood volume
that further increases ICP. Paradoxically, this further
reduces cerebral perfusion pressure producing a
feedback cycle that results in the total reduction of
cerebral flow and perfusion. The result of this feedback
loop is cerebral ischemia and brain infarction with
neuronal death. In cases where intracranial
hypertension is the result of hemorrhage, increased
blood pressure will worsen intracranial bleeding, thus
worsening intracranial hypertension.

11. History and Physical
• Symptoms of elevated intracranial hypertension are primarily derived
from neurological irritation, compression, or displacement, and
papilledema. Non-specific headaches are recorded in almost all cases
and are likely mediated via the pain fibers of the trigeminal nerve in
the dura and blood vessels of the brain. Pain is generally diffuse and
worse in the mornings with exacerbation by the Valsalva maneuver.
Nausea and vomiting are common presentations of elevated ICP.
Patients can present with double vision most frequently with
horizontal diplopia associated with sixth cranial nerve palsy from
compression. Transient visual abnormalities occur frequently, often
described as a gradual dimming of vision in one or both of the eyes.
Visual abnormalities worsen with changes in posture. Peripheral
visual loss may be reported and most commonly begins in the nasal
inferior quadrant with subsequent loss of the central visual field.
Alterations in visual acuity with blurring or distortion may occur.
Variable degrees of loss of color distinction may occur. In more severe
or chronic cases, a sudden visual loss can occur due to intraocular
hemorrhage.

12. • Tinnitus with a pulsing rhythm exacerbated by supine or
bending positions and Valsalva maneuvers can occur.
Radicular pain, numbness, or paresthesias are possible and
most commonly associated with localized compression or
possible herniation of the brain. Neurological findings are
indications of severe disease. The anatomical locations
where the herniation is most likely to occur include the
subfalcine, central transtentorial, uncal transtentorial,
cerebellar tonsillar/foramen magnum, and transcalvarial
routes. These types of changes may lead to decreased
consciousness or responsiveness. Focal neurological
constellations depend on which region of the brain has
herniated. Often this results in a stupor state or more
severely with coma due to the local effect of mass lesions or
pressure on the reticular formations of the midbrain. It may
further lead to respiratory compromise.

13. • Physical exam findings can vary widely depending on
etiology. A change in mental status or comatose patient
should be promptly evaluated. A complete neurological
assessment is essential whenever intracranial hypertension
is suspected. Cranial nerve assessment is particularly
important for identifying lesions. Sixth cranial nerve palsy is
most common. Blunting of the pupillary reflex with fixed
dilation of one pupil is also highly associated with herniation
syndromes. Spontaneous periorbital bruising may be present
as well. A classic triad of bradycardia, respiratory depression,
and hypertension is known as the Cushing triad and is highly
indicative of intracranial hypertension. Fundoscopic
examination looking for retinal hemorrhages or papilledema
is essential. Alterations in respiratory drive and effort may
occur leading to failure of respiration and oxygenation.
• Infants can have a widening of cranial sutures and bulging
fontanelle.

14. Evaluation
• Complete blood count (CBC) and complete metabolic panel
(CMP) are usually checked in all patients with suspected
intracranial hypertension to evaluate for infection, anemia,
and electrolyte abnormalities. The initial evaluation should
include a head computed tomography (CT) scan. CT scan
findings of cerebral edema such as compressed basal
cisterns and midline shift are predictive of elevated ICP.
However, the absence of these findings does not rule out
intracranial hypertension. A head MRI is more accurate
than a head CT in evaluating elevated ICP and looking for
potential etiology. Bedside ultrasonography also can be
used to measure the diameter of the optic nerve sheath to
determine intracranial hypertension. However, this study is
limited by operator skill and not frequently used.

15. • A lumbar puncture (LP) may sometimes be needed for
diagnosis. However, it should be delayed until
neuroimaging, especially in those with suspicion of
impending herniation. When LP is performed, in addition to
measuring opening pressures, CSF should also be tested for
infection and other potential etiology. Invasive
measurement of ICP is definitive for diagnosis and improves
the provider’s ability to maintain adequate cerebral
perfusion pressure (CPP). There are four main anatomical
sites used for clinical measurement of intracranial pressure:
intraventricular, intraparenchymal, subarachnoid, and
epidural. A ventriculostomy catheter is the preferred device
for ICP monitoring and can be used even for therapeutic CSF
drainage to lower ICP. When ventricles cannot be
cannulated, intraparenchymal devices using microsensors
and fibreoptic transducers may be used. Subdural and
epidural monitors are not as accurate as ventriculostomy
and parenchymal monitors

16. Treatment / Management
• Treatment of chronic intracranial hypertension is mainly
focused on treating and reversing the etiology.
• A sudden increase in ICP is a neurosurgical emergency,
requiring close monitoring in an intensive care unit (ICU)
setting. For acute intracranial hypertension, a patient
should first be stabilized with healthcare providers aiming
for hemodynamic stability, and preventing and treating
factors that may aggravate or precipitate intracranial
hypertension. These patients should have close monitoring
of heart rate, blood pressure, body temperature,
ventilation and oxygenation, blood glucose, input and
output, and ECG. Patients with suspected intracranial
hypertension, especially with severe traumatic brain injury,
should also have ICP monitoring

17. • It is vital to prevent and treat factors that may
aggravate or precipitate intracranial hypertension.
These interventions are used to buy time until the
underlying etiology is identified and corrected.
• Keep the head elevated to 30 degrees and neutrally
positioned to minimize venous outflow resistance and
improve cerebral spinal fluid displacement from the
intracranial to the spinal compartment.
• Hypoxia and hypercapnia can increase ICP. Controlling
ICP through optimal respiratory management is crucial.
It is essential to control ventilation to maintain a
normal partial pressure of carbon dioxide (PaCO2) and
maintain adequate oxygenation without increasing the
PEEP.

18. • Agitation and pain can increase blood pressure and ICP.
Adequate sedation and analgesia is an important
adjunctive treatment. Since most sedating medications
can have effects on blood pressure, medications with a
minimal hypotensive effect should be preferred.
Hypovolemia can precipitate the hypotensive side
effects and should be treated before administering
sedative agents. Shorter-acting agents have the
advantage of allowing brief interruption of sedation to
evaluate neurological status.
• Fever can increase brain metabolic rate and is a potent
vasodilator, which in turn increases the cerebral blood
flow and leads to an increased ICP. Fever should be
controlled with antipyretics and cooling blankets and
infectious causes must be ruled out.

19. • Elevated blood pressure is commonly seen in patients with
intracranial hypertension especially when due to traumatic
brain injury. In patients with untreated intracranial mass
lesions, cerebral perfusion is maintained by the higher
blood pressure, and systemic hypertension should not be
treated. The absence of an intracranial mass lesion
presents a more individualized, controversial decision when
treating systemic hypertension. When antihypertensive
drugs are used, the preferred treatment includes beta-
blockers like labetalol and esmolol or calcium channel
blockers because they reduced blood pressure without
affecting ICP. Agents with short half-lives should be
preferred. Avoid vasodilators like sodium nitroprusside,
nitroglycerin, and nifedipine.
• Seizures can contribute to and complicate elevated ICP and
should be prevented by prophylactic medications,
especially in severe traumatic brain injuries.

20. For patients with sustained intracranial
hypertension, additional measures are
needed to control the ICP.
• Emergent surgical management should be
considered when there is sudden intracranial
hypertension or refractory to medical
management.
• Nondepolarizing muscle relaxants along with
sedatives may be used to treat intracranial
hypertension caused by posturing, coughing, or
agitation. When a neuromuscular blockade is used,
EEG should be monitored to rule out convulsive
states.
• Hyperosmolar therapy is used for severe, acute
intracranial hypertension.

21. • Mannitol is commonly used as a hyperosmolar agent
and is usually given as a bolus of 0.25 to 1 g/kg body
weight. Serum osmolality should be kept less than 320
mOsm to avoid side effects of therapy like renal failure,
hypokalemia, and hypo-osmolarity.
• Hypertonic saline can also create an osmotic shift from
the interstitial space of brain parenchyma into the
intravascular compartment in the presence of an intact
blood-brain barrier. Hypertonic saline has an advantage
over mannitol for hypovolemic and hypotensive
patients. The adverse effects of hypertonic saline
administration include hematological and electrolyte
abnormalities. Hyponatremia should be excluded
before administering hypertonic saline to reduce the
risk of central pontine myelinolysis.

22. • Hyperventilation can be used for a rapid reduction in ICP if
there are clinical signs of herniation or with severe
intracranial hypertension. Hyperventilation decreases PaCO2
which causes vasoconstriction of cerebral arteries, resulting
in reduced cerebral blood flow and reduced intracranial
pressure.
• Barbiturate coma should be considered for patients with
refractory intracranial hypertension.
• Routine induction of hypothermia is not indicated; however,
moderate hypothermia may be an effective adjunctive
treatment for increased ICP refractory to other medical
management.
• Steroids are commonly used for primary and metastatic
brain tumors to decrease vasogenic cerebral edema. For
other neurosurgical disorders like traumatic brain injury or
spontaneous intracerebral hemorrhage, steroids have not
been shown to benefit and sometimes may even be
detrimental.

23. Surgical Interventions
• Resection of intracranial mass lesions producing
elevated ICP should be done as soon as possible.
• CSF drainage lowers ICP immediately by reducing
intracranial volume. This modality can be an important
adjunct treatment for lowering ICP. However, it has
limited utility when the brain is diffusely swollen and
the ventricles are collapsed.
• Decompressive craniectomy is used to treat severe
uncontrolled intracranial hypertension. It involves
surgical removal of part of the calvaria to create a
window in the skull, allowing for herniation of swollen
brain through the bone window to relieve pressure.

24. Differential Diagnosis
• Intracranial hypertension can occur in different diseases. Following
conditions should be considered when patients with intracranial
hypertension are encountered.
• Acute nerve injury
• Benign intracranial hypertension (Pseudotumor cerebri)
• Cerebrovascular ischemia/hemorrhage
• Hydrocephalus
• Intracranial epidural abscess
• Intracranial hemorrhage
• Leptomeningeal carcinoma
• Low-grade astrocytoma
• Lyme disease
• Meningioma
• Meningitis
• Migraine headache
• Papilledema
• Subarachnoid hemorrhage
• Venous sinus thrombosis

25. Prognosis
• Prognosis is highly variable depending on etiology
and varies from benign to lethal. Children usually
can tolerate higher intracranial pressure (ICP) for
a longer period. Idiopathic intracranial
hypertension (IIH) is not associated with any
specific mortality risk but surgical treatments may
cause morbidity and mortality. The morbidity of
IIH is related to effects on visual function due to
papilledema. If not treated disc edema can cause
irreversible optic neuropathy, and loss of color
vision.

26. Complications
• Complications of intracranial hypertension
depend on the underlying etiology. Some
general dreadful complications are:
• Stroke
• Seizures
• Optic neuropathy
• Loss of vision
• Stupor, coma
• Respiratory arrest

27. Meningeal syndrome

28. • Meningism is a set of symptoms similar to those
of meningitis but not caused by meningitis, it’s is
caused by nonmeningitic irritation of the meninges,
usually associated with acute febrile illness, especially
in children and adolescents.
• Meningeal syndrome is a complex of subjective and
objective symptoms arising from iritaion of the
meninges pathologicaly.
• Meningitis is a disease caused by the
inflammation of the protective membranes covering
the brain and spinal cord known as the meninges.

29. Etiology
• The most common evoking factors are:
• neuroinfection;
• subarachnoid hemorrhage;
• tumors − especially meningic carcinomatosis
(difuse tumor infiltration of meninges).
• Another cause can be for example lesion of
the brain tissue etc.

30. Clinically
• Meninges irritation leads to irritation of the
nerve roots (passing through meninges) and
to contraction of the neck and paravertebral
muscles. Typically the patient has tilted head
back, lies on their back with flexed lower
limbs, states subjective meningeal symptoms
and they also can be proved.

31. Subjective meningeal symptoms
• headache – typically difused;
• vomiting;
• photo- and phonofobia;
• hyperesthesia;
• fever;
• in advanced stages also qualitative and
quantitative disorders of consciousness.
• Variably can be nausea and stiff neck.

32. Objective meningeal symptoms
Kernig sign
patient is kept in supine position, hip and knee are
flexed to a right angle, and then knee is slowly
extended by the examiner. The appearance of
resistance or pain during extension of the patient's
knees beyond 135 degrees constitutes a positive
Kernig's sign.
• Kernig in his original description did not consider
pain as a required component of the maneuver;
however, many clinicians include pain as an
essential component of a positive sign.

33. Brudzinski's neck sign
• is performed with the patient in the supine
position. To elicit this maneuver, the
examiner keeps one hand behind the
patient's head and the other on chest in
order to prevent the patient from rising.
Reflex flexion of the patient's hips and knees
after passive flexion of the neck constitutes
a positive Brudzinski sign

34. Usefulness and limitations of these signs
• Sensitivity of both the signs for the diagnosis of
meningitis/meningeal syndrome has been reported
quite low.
• sensitivity of meningeal signs are not proportionate
to the disease severity in patients with moderate or
severe meningeal inflammation or with
microbiological evidence of central nervous system
infection.
• Irrespective of disease severity, these meningeal
signs may be absent in infants or elderly patients, in
immunocompromised or comatose patients. All
these factors may account for low sensitivity.

35. • From the figures and studies mentioned
above, it is apparent that both, Kernig's
and Brudzinski's signs, are not very
sensitive for detecting meningitis and,
therefore, when absent, should not be
inferred as there is no evidence of
meningitis. Although the sensitivity is
quite low, the high specificity suggests that
if Kernig's or Brudzinski's sign is present,
there is a high likelihood for meningitis or
meningeal syndrome.

36. Diagnosis
• Lumbar punction and examination of
cerebrospinal fluid;
• CT − in suspicion of a subarachnoidal
hemorrhage, inflammatory deposits can be
displayed

37. Diagnostic search algorithm in the
patient with meningeal syndrome.

38. Literature
• https://www.ncbi.nlm.nih.gov/books/NBK507
811/#:~:text=Intracranial%20hypertension%2
0is%20a%20spectrum,increased%20intracrani
al%20pressure%20(ICP).
• https://thecontentauthority.com/blog/mening
ism-vs-meningismus
• https://www.cdc.gov/meningitis/index.html