Test: Raised ICP- 1 - NEET PG MCQ

The image depicts a halo or target sign, characterised by a distinct ring encircling a central bloody spot after bloody nasal discharge is placed on a handkerchief or paper towel.
Beta trace protein is present in cerebrospinal fluid (CSF) and is synthesised by the meninges and choroid plexus.

• It exhibits Prostaglandin D₂ synthase activity.
• The concentration is 1.5 mg/L in ventricular CSF.

It is important to note that Beta 2 micro-globulin levels are assessed in urine to evaluate the prognosis of patients with multiple myeloma.

Opening eyes on command - 3.

• Moving limbs/obeying commands = 6.
• Intubated = T.

The overall score is 9T. The highest score for an intubated patient can be 10T, while the lowest is 2T.
Glasgow coma scale- P
The GC5-P is calculated by subtracting the Pupil Reactivity Score (PR5) from the glasgow come scale (GCS) total score:
- GCS - P = GCS - PRS
The pupil reactivity score is calculated as follows.
Pupils unreactive to light-Pupil reactivity score

• Both pupiis-2
• One pupil-1
• Neither pupil-0

• Spontaneous eye opening is assigned a score of 4.
• The patient can localise pain, which is evident as he moves his arm away from the painful stimulus, earning a score of 5.
• Using inappropriate words results in a score of 3.
• Therefore, the cumulative score is 12.

TABLE: Glasgow coma scale for head injury
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The primary risk factor for cortical vein thrombosis is a prothrombotic condition, such as pregnancy and the puerperium. Patients typically present with:

• Headaches that may start gradually or suddenly (thunderclap onset) and exhibit signs of increased intracranial pressure (ICP).
• Headaches that can occur with or without focal neurological deficits, depending on the affected area.
• Possible cranial nerve palsies.

Magnetic resonance venography is the most effective imaging technique. Meningitis can be excluded due to the lack of meningeal signs. Migraine is also ruled out because it does not present with raised ICP or papilledema. Subarachnoid haemorrhage (SAH) typically manifests as a thunderclap headache accompanied by meningeal signs.

Opening eyes in response to pain is scored as E2.
Moaning indicates incomprehensible sounds and is given a score of V2.
The ability to localise pain is rated as M5.
Therefore, the overall score for the patient is 9.

A positive Kernig sign indicates meningeal irritation rather than increased intracranial pressure (ICP). Ipsilateral hemiplegia arises from the Kernohan-Woltman sign observed in uncal herniation. The pupil on the same side as the central nervous system (CNS) bleed expands and exhibits a delayed response to light. This phenomenon is associated with uncal herniation and is referred to as Hutchinson's pupil. Additionally, blurring of the disc margins is an early indicator of papilledema.

Neuroimaging is recommended before performing a lumbar puncture (LP) in the following cases:

• Altered level of consciousness
• Focal neurological deficit
• New onset seizure
• Papilledema
• Immunocompromised state

Patients in these categories face a heightened risk of potentially lethal cerebellar or tentorial herniation after a lumbar puncture. Options B, C, and D meet the criteria outlined above.

In brain death, the brain stem is no longer functioning, yet the spinal cord remains intact. Therefore,

• Deep tendon reflexes can still be triggered.
• The Babinski sign may be observed on both sides.

The gag reflex is absent because of harm to the medulla. Pupils are dilated and do not respond to light due to injury in the midbrain. To confirm a diagnosis of brain death, it is essential to exclude:

• Effects of sedatives
• Hypothermia
• Neuromuscular paralysis

If there is uncertainty, cerebral blood flow studies and an EEG should be performed.

Foraminal brain herniation results in the compression of the medulla, which can lead to respiratory arrest.

• Third nerve palsy can cause ipsilateral pupillary dilatation and ipsilateral hemiplegia, particularly in uncal (midbrain) herniation.
• The Locked In state arises from a lesion in the ventral pons.

• Elevate the head end
• Drain CSF through ventriculostomy
• Administer osmotherapy using mannitol
• Utilise glucocorticoids for vasogenic oedema (avoid in cases of head injury and stroke)
• Provide sedation with morphine, propofol, or midazolam, and neuromuscular paralysis if required
• Perform hyperventilation to maintain PaCO₂ at 30-35 mm Hg; this should be for short-term use or omitted due to limited effectiveness
• Initiate pressor therapy with phenylephrine, dopamine, and norepinephrine to ensure a CPP of more than 60 mm Hg
• Consider second-tier therapies:
  • Decompressive craniectomy
  • Pentobarbital coma
  • Therapeutic hypothermia to 33 degrees

• According to stepwise management of raised ICP as outlined by Harrison, sedation is administered prior to hyperventilation. Moreover, hyperventilation is noted as a short-term measure or one that may be skipped.
• Bradley’s textbook of neurology states that elective hyperventilation does not lead to a reduction in CO₂.
• The BTF 2016 guidelines indicate that 'hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often critically reduced.'

Typically, between 20 and 30 ml of CSF can be safely extracted from adults. This fluid is utilised for:

• Cell counts with differential analysis
• CSF biochemistry
• Culturing
• Smears
• PCR
• Immune-electrophoresis
• Oligoclonal banding
• Cytology

CSF should be allowed to flow into collection tubes rather than being drawn out using a syringe.

• A lumbar puncture extracting 25-40 ml of CSF, while monitoring opening and closing pressures.
• Objective evaluation by comparing videotaped gait of the patient both prior to and following the procedure.

• Multiple lumbar punctures conducted over 3-5 days
• Placement of a continuous lumbar CSF drain
• Radionuclide cisternography

• The presence of dementia, gait issues, and urinary incontinence leans towards normal pressure hydrocephalus.
• Biswanger's disease is linked to hypertension, which this patient does not exhibit.
• This condition results in vascular dementia.
• Accompanying white matter lesions can cause pyramidal signs.
• Parkinsonian rigidity may also be observed.

• Visual hallucinations
• REM sleep disorder
• Capgras syndrome

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• The rarer occurrence of arm extension combined with limb flexion is associated with lesions in the pons.

Alpha rhythm displays a discharge frequency ranging from 8 to 13 Hz. Upon eye opening, this pattern transitions to beta rhythm.

In cases of pontine or diffuse cortical anoxia, a unique pattern of alpha coma is characterised by:

• Extensive alpha rhythm
• Resemblance to the normal rhythm
• No change in response to environmental stimuli

Drowsiness and stupor may arise due to the horizontal movement of the diencephalon (Thalamus). The lateral displacement can be assessed using a CT scan or MRI. In the event of a rapidly enlarging mass, the horizontal displacement of pineal calcification is evaluated:

• Displacement of 3 - 5 mm correlates with drowsiness.
• Displacement of 6 - 8 mm correlates with stupor.
• Displacement greater than 9 mm correlates with coma.

Glucocorticoids are beneficial for managing vasogenic oedema resulting from tumours or brain abscesses. However, they are not recommended in cases of:

• Head trauma
• Ischemic stroke
• Haemorrhagic stroke

Neither norepinephrine nor pressor therapy is employed to maintain MAP in order to keep CPP > 60 mm Hg. Sedation is achieved using propofol or midazolam. Neuro-muscular paralysis will be required, and the patient will need ventilatory support. This approach will help secure the airway and maintain pCO₂ between 30 - 35 mm Hg.

The most prevalent type of brain herniation is trans-tentorial herniation. This condition involves the displacement of brain tissue from the supratentorial to the infratentorial compartment. This type of brain herniation can be categorised into:

• Uncal trans-tentorial herniation: This occurs when the medial temporal gyrus is pushed into the tentorial opening, located just anterior to and adjacent to the midbrain. It results in ipsilateral third nerve palsy accompanied by ipsilateral hemiplegia, known as the Kernohan-Woltman sign.
• Central trans-tentorial herniation: This involves the symmetric downward movement of thalamic structures through the tentorial opening, leading to compression of the midbrain. It manifests as miotic pupils and stupor.

Transfalcial herniation arises from the displacement of the cingulate gyrus beneath the falx and across the midline. In contrast, the downward displacement of cerebellar tonsils into the foramen magnum is referred to as foraminal herniation. This condition results in the compression of vital centres within the brain.

• Pointer A: Uncal herniation.
• Pointer B: Central herniation.
• Pointer C: Transfalcial herniation.
• Pointer D: Foraminal herniation.

Patients diagnosed with Benign Intracranial Hypertension/Idiopathic Intracranial Hypertension (IIH) typically exhibit symptoms associated with elevated intracranial pressure (ICP) and papilledema. These symptoms encompass:

• Headache
• Transient visual disturbances
• Diplopia resulting from unilateral or bilateral abducens nerve palsy

As a result, options B and D are excluded.
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Glasgow Coma Scale
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Glasgow Coma Scale Update

• The GCS score is derived by assigning notation to the level In each of the three subcomponents of the GCS and summing the results of a patient's assessment. Further Information on the GCS score can be accessed here. The Pupil Reactivity Score summarises Information about of pupil reactivity to light and is calculated as follows:
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The GCS-P is calculated by subtracting the pupil reactivity score (PRS) from the Glasgow Coma Scale
GCS - P = GCS - PRS
Minimum score 3, Max score 15
Intubation indicated when score less than 8.

The preferred type of shunt is a ventriculo-peritoneal shunt, which features a one-way valve that can control intra-cranial pressure. This device facilitates the drainage of CSF into the peritoneal cavity.

The history of repetitive blanking out, accompanied by subtle motor activities like lip quivering, is indicative of the presence of absence seizures. Characteristics of absence seizures include:

• Sudden, brief lapses in consciousness without a loss of postural control.
• Typically lasts only for a few seconds, with consciousness returning just as abruptly as it was lost, and no postictal confusion.
• Often associated with subtle bilateral motor signs, such as rapid eyelid blinking, chewing movements, or small clonic movements of the hands.
• Due to the subtle nature of the clinical signs, especially to parents, the initial indication of absence epilepsy is frequently unexplained 'daydreaming' and a noticeable decline in school performance observed by a teacher.
• The electrophysiological hallmark of typical absence seizures is a generalized, symmetric, 3-Hz spike-and-wave discharge that commences and concludes suddenly, superimposed on a normal EEG background, and can be triggered by hyperventilation and photic stimulation.

The Glasgow Coma Scale comprises three components:

• Eye opening
• Verbal response
• Motor activity

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• Idiopathic intracranial hypertension is commonly seen in obese women, presenting with headaches and sixth cranial nerve palsy.
• Optic neuritis is an acute inflammatory disorder affecting the optic nerve, resulting in painful eye movements and vision loss.
• The fundus appears normal due to retro-bulbar pathology.
• Sagittal sinus thrombosis arises in the context of risk factors including OCP, pregnancy, the post-partum period, polycythaemia, and APLAS.

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