Test: Raised ICP- 2 - NEET PG MCQ

• hypertension
• bradycardia
• irregular respirations (such as Cheyne-Stokes breathing)

• Subdural hematoma presents as a concavo-convex hyper-density.
• Extradural haemorrhage appears as a biconvex or flame-shaped hyper-density.
• Subarachnoid haemorrhage occurs alongside intra-ventricular bleeding or blood located in the Sylvian fissure.
• Intra-parenchymal bleeding is typically a lesion or hyper-density found in the basal ganglia, often resulting from hypertension.

Extradural hemorrhage: Bleeding takes place between the skull and the dura mater. This bleeding results from the rupture of the middle meningeal artery. A lucid interval, defined as consciousness between two episodes of unconsciousness, can be observed. An NCCT scan of the head reveals hyperdensity that is bi-convex or flame-shaped.

Subdural hemorrhage: This type of hemorrhage occurs due to the rupture of cortical bridging veins. On an NCCT scan, it presents as a concavo-convex or sickle-shaped bleed.

In uncal or midbrain herniation, the elevated ICP exerts pressure on the ipsilateral third cranial nerve as it arises from the Edinger-Westphal nucleus. This results in:

• Ptosis
• Diplopia
• Divergent squint

The cause of unconsciousness may be attributed to damage to the reticular activating system located in the midbrain.

The Aqueduct of Sylvius links the third ventricle to the fourth ventricle. As a result, any blockage in this region will not only lead to an enlargement of the third ventricle but will also cause dilation of the lateral ventricles that are close to the obstruction.

​
Papilledema: Accompanied by a blurring of the edges of the optic disc.

• Bradycardia
• Hypertension (accompanied by widened pulse pressure)
• Bradypnea (often irregular)

Increased ICT results in bradycardia accompanied by hypertension. Uncal herniation of the brain causes ipsilateral pupillary dilatation. A decrease in GCS due to damage to the reticular activating system results in the onset of coma. The effective operation of the R.A.S system, its ascending pathways to the cortex, and the cortex itself are essential for sustaining alertness and coherent thought. Thus, the main causes of coma include:

• Lesions that harm the RAS in the upper midbrain or its projections
• Destruction of significant areas of both cerebral hemispheres
• Suppression of reticulo-cerebral function by substances, toxins, or metabolic disturbances such as hypoglycaemia, anoxia, uraemia, and liver failure

Pupillary dilation with the absence of light response, along with the loss of vertical and adduction eye movements, indicates a lesion in the upper brainstem. In contrast, the maintenance of pupillary light reflex and eye movements suggests that the upper brainstem is unaffected, pointing to widespread structural lesions or metabolic suppression of the cerebral hemispheres as the cause of coma.

Criteria for brain death encompass three crucial components:

• Extensive cortical damage, indicated by profound coma and lack of response to all types of stimulation.
• Global brainstem injury, evidenced by the absence of pupillary light reflex and the loss of both oculovestibular and corneal reflexes.
• Destruction of the medulla, shown by total apnea.

Apnea testing can be conducted safely using diffusion oxygenation before the ventilator is removed. This involves:

• Pre-oxygenation with 100% oxygen, maintained throughout the test via a tracheal cannula.
• A CO₂ tension increase of 0.3 - 0.4 kPa/min (2 - 3 mmHg/min) during apnea.

At the conclusion of a monitoring period, usually lasting several minutes, arterial pCO₂ must be greater than 6.6 - 8.0 kPa (50 - 60 mmHg) for the test to be considered valid. Apnea is confirmed if no respiratory effort is evident despite a significantly elevated Pco2. The loss of deep tendon reflexes is not necessary, as the spinal cord remains operational.

• In most current paediatric protocols, cranial irradiation (12 to 18 Gy) is administered to 5% to 25% of patients—specifically those with T-cell ALL, evident CNS disease (CNS3 status), or high-risk cytogenetics.
• Typically, blasts are not detected in CSF, and the presence of a single blast in CSF indicates potential CNS involvement.

An enlarged and poorly reactive pupil indicates either compression or stretching of the third cranial nerve due to a cerebral mass above. The most severe pupillary sign, which is characterised by bilaterally dilated and unresponsive pupils, suggests significant midbrain injury, typically resulting from compression by a supratentorial mass. Midsize pupils that are reactive and round (2.5 – 5 mm) generally rule out a midbrain lesion.

• The doll's eye reflex, also known as oculocephalic reflexes, is triggered by moving the head sideways or vertically while observing the eye movements in the opposite direction of the head movement. This reflex relies on the integrity of the ocular motor nuclei and their connecting tracts that extend from the midbrain to the pons and medulla. These movements, sometimes inappropriately termed 'doll's eyes', are usually suppressed in a conscious patient. The absence of the oculocephalic reflex, referred to as the presence of doll's eye reflex, indicates cerebral dysfunction.
• Regarding Horner's pupil: A patient with Horner's syndrome exhibits a weakened dilator muscle in one iris due to diminished sympathetic activity, resulting in that pupil dilating more slowly than the unaffected one. If the sympathetic lesion is complete, the affected pupil will only dilate through sphincter relaxation. This leads to an asymmetry in pupil dilation, known as anisocoria, which is most pronounced 4–5 seconds after the lights are turned off; this process is significantly slower than commonly perceived.
• Positive vestibulo-cochlear reflexes occur when thermal or caloric stimulation of the vestibular apparatus (oculo-vestibular response) is performed by irrigating the external auditory canal with cool water, creating convection currents in the labyrinths. Following a brief latency, this results in a tonic deviation of both eyes towards the side of the cool water irrigation and nystagmus in the opposite direction. The absence of induced conjugate ocular movements suggests possible brainstem damage.

Pseudotumour cerebri (also known as benign intracranial hypertension) primarily affects young, obese females. It is diagnosed through exclusion, following neuroimaging to eliminate the presence of intracranial lesions. Investigations include:

• Assessing for fundus papilledema.
• Conducting an MR angiogram in selected cases to investigate potential dural venous sinus occlusion or arteriovenous shunt.
• If neuroimaging results are negative, measuring the subarachnoid opening pressure via lumbar puncture (LP).
• An increased pressure with normal cerebrospinal fluid (CSF) suggests pseudotumour cerebri (idiopathic intracranial hypertension).

Risk factors include:

• Obesity: Women under 44 who are obese are almost 20 times more likely to develop this condition.
• Medications that can induce pseudotumour cerebri:
  • Growth hormone,
  • outdated tetracycline,
  • discontinuation of steroids,
  • excessive vitamin A,
  • and oral contraceptives.

Treatment options consist of:

• Providing temporary relief by draining 20-30 ml of CSF via lumbar puncture (both diagnostic and therapeutic).
• Using acetazolamide to decrease CSF production.
• Encouraging weight loss.
• Implementing a shunt if previous measures fail and visual loss progresses.
• Conducting emergency surgery if there is a sudden onset of blindness due to severe papilledema.

The patient has a background of gastrointestinal bleeding presenting as melena, likely triggered by an aspirin-induced gastric ulcer.

• Hypotension and tachycardia support this diagnosis.
• A cerebrovascular accident (CVA) is linked with bradycardia and hypertension due to increased intracranial pressure (ICP).
• To ensure brain perfusion, the Cushing's reflex is activated.

There is no indication of septic shock in the clinical details provided.

• The nearest possibility to exclude is myocardial infarction (MI) with cardiogenic shock.
• The history of fainting is mentioned, but there is no reference to chest pain or ECG results in the question.

Eye opening (E), Verbal response (V), and Best motor response (M) are the components of the GCS score. This score is determined by assigning values to each of the three subcomponents and then adding the results from a patient's evaluation. The Pupil Reactivity Score provides a summary of how pupils respond to light, calculated as follows:

• Pupils unreactive to light: 0
• Both pupils reactive: 2
• One pupil reactive: 1
• Neither pupil reactive: 0

The GCS-P is derived by deducting the pupil reactivity score (PRS) from the Glasgow Coma Scale. Thus, GCS - P = GCS - PRS.

• To avert additional neuronal death (known as secondary brain injury), it is essential to restore the flow of well-oxygenated blood.
• The optimal level of cerebral perfusion pressure (CPP) should be at least 50-70 mm Hg.
• Mortality rises by approximately 20% for every 10 mm Hg decrease in CPP.
• In studies where CPP is maintained above 70 mm Hg, mortality reduction can reach up to 35% for patients with severe head injuries.

Acetazolamide is regarded as the most effective medication for reducing ICP in idiopathic intracranial hypertension. Most individuals find significant relief from symptoms, particularly headaches, when using this primary treatment.
If a patient cannot tolerate acetazolamide, furosemide can serve as a substitute diuretic for this group.
Those with IIH may suffer from headaches resembling migraines. These can often be effectively managed with:

• amitriptyline
• propranolol
• other widely used migraine prophylactic medications

Patients noticing a progressive loss of visual field in one or both eyes should be promptly placed on high-dose oral prednisone (60-100 mg/day) or an equivalent corticosteroid regimen.
Despite thorough follow-up care and optimal medical treatment, some patients may experience a decline in their visual function. In such cases, surgical options may be explored:

• Optic nerve sheath fenestration (decompression)
• Cerebrospinal fluid (CSF) diversion, such as through a lumboperitoneal or ventriculoperitoneal shunt

Uncal Herniation Manifestations

1. Subtype of trans-tentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the midbrain.
2. The uncus can squeeze the third cranial nerve, which may affect the parasympathetic input to the eye on the side of the affected nerve, causing the pupil of the affected eye to dilate and fail to constrict in response to light as it should.
3. Pupillary dilation often precedes the somatic motor effects of cranial nerve III compression. The symptoms occur in this order because the parasympathetic fibers surround the motor fibers of CNIII and are hence compressed first.
4. False localizing sign, the so-called Kernohan’s notch, which results from compression of the ipsilateral cerebral crus containing descending cortico-spinal and some corticobulbar tract fibers. This leads to ipsilateral hemiparesis (as these tracts are above their decussation where they are compressed
5. Distortion of the brainstem leading to Duret hemorrhages in the median and paramedian zones of the mesencephalon and pons.
6. The disrupted brainstem can lead to decorticate posture, respiratory center depression and death. Other possibilities resulting from brain stem distortion include lethargy, slow heart rate, and pupil dilation.
7. Compression of the ipsilateral posterior cerebral artery will result in ischemia of the ipsilateral primary visual cortex and contralateral visual field deficits in both eyes (contralateral homonymous hemianopsia).

In the paediatric population, vitamin A toxicity may manifest as pseudotumour cerebri. While steroids are utilised in the treatment of this condition, abruptly discontinuing them can result in a deterioration of symptoms.

• Most instances of idiopathic intracranial hypertension (IIH) are found in young women who are overweight.
• A significantly smaller fraction occurs in otherwise healthy men.
• Individuals with elevated body mass indexes (BMIs) and recent weight gain face a heightened risk.

Normal ICP ranges from 50-80 mm of water, which converts to approximately 3.6 to 5.8 mm Hg. Therefore, the answer is: < 5 mm Hg.

If the query pertains to cerebral perfusion pressure in children, it should be 45 mm Hg, whereas in adults it must be at least 70 mm Hg.

ICP Waveforms:

• A waves or plateau waves - These feature a rapid increase in ICP from nearly normal levels to 50 mm Hg or higher, lasting for 5 to 20 minutes before dropping sharply. They are always pathological and signify significantly reduced compliance. These waves often accompany neurological decline and indicate early brain herniation.
• B waves - These rhythmic oscillations occur every 1 to 2 minutes. ICP increases in a crescendo pattern to levels 20-30 mm Hg above baseline before falling abruptly. Initially, these waves were always linked to Cheyne-Stokes respiration. However, they can also be seen in ventilated patients and are likely associated with variations in cerebrovascular tone and cerebral blood volume. B waves indicate failing intracranial compensation and suggest cerebral vasospasm.
• C waves - These oscillations happen at a frequency of 4-8 per minute and have a smaller amplitude compared to B waves. They are synchronised with spontaneous Traub-Hering-Meyer type fluctuations in blood pressure and are likely of limited pathological importance.

Indications In E/R for Burr Hole:
Clinical criteria are based on a worsening neurological examination.

• Patient experiencing rapid trans-tentorial herniation.
• Brainstem compression that fails to improve or stabilise with mannitol and hyperventilation.

Indicators of transtentorial herniation/brainstem compression include:

• A sudden decrease in Glasgow Coma Scale (GCS) score.
• One pupil is fixed and dilated.
• Paralysis or decerebration, usually contralateral to the dilated pupil.

Recommended scenarios for applying these criteria:

• A neurologically stable patient experiences witnessed deterioration as described above.
• An awake patient undergoes a similar process during transport, with changes well documented by qualified medical or paramedical personnel.

Choice of Side for the initial Burr Hole:
Start with a temporal burr hole on the side:

• Ipsilateral to the dilated pupil. This will be on the correct side in over > 85% of cases of epidurals and other extra-axial mass lesions.
• If both pupils are dilated, use the side of the first dilating pupil (if known).
• If pupils are equal, or if it is unclear which side dilated first, position the hole on the side of evident external trauma.
• If there are no localising clues, place the hole on the left side to evaluate and decompress the dominant hemisphere.

Hydrocephalus ex vacuo pertains to the expansion of cerebral ventricles and subarachnoid spaces, typically resulting from brain atrophy, which can occur in conditions such as dementias or following post-traumatic brain injuries.

• This condition differs from hydrocephalus in that it involves a compensatory enlargement of the CSF spaces.
• This enlargement is a response to the loss of brain parenchyma.
• It does not occur due to elevated CSF pressure.

• Following bolus administration, it increases circulating volume, reduces blood viscosity, and enhances cerebral blood flow as well as oxygen delivery to the brain.
• Its osmotic effects manifest within 15 to 30 minutes, establishing an osmotic gradient that extracts water from neurons.

• For instance, patients exhibiting signs of imminent herniation (such as a unilateral dilated pupil or extensor posturing) or those with an enlarging mass lesion may find mannitol beneficial for promptly lowering ICP while awaiting CT scanning or surgical intervention.

• Intubated individuals with treatment commenced within 6 hours post-cardiac arrest (non-perfusing ventricular tachycardia [VT] or VF).
• Patients who can sustain a systolic blood pressure of >90 mm Hg, whether or not they are on pressors, after CPR.

• Cardiac arrest - supported by clinical studies.
• Ischemic stroke - clinical trials have only been reported in animal studies, as per Harrison's and online sources.
• Traumatic brain or spinal cord injury without fever - confirmed by clinical studies.
• Neurogenic fever following brain trauma - validated by clinical studies.