Case 1 Cervical disc prolapse

Figure 1: MRI brain of the patient sagittal T2 sequence and axial T2.

Clinical presentation

• Female pt. 53 years old with 9 months history of bilateral brachialgia more on the right side with diffuse distribution.
• The condition started after significant head trauma.
• 3 months ago, the patient developed quadriparesis, difficulty walking associated with urine incontinence.
• MRI shown in figure 1-1.

 

• Q1: What are the main categories of presentation for cervical disc prolapse CDP? Into which of these categories could this patient be classified?”
• The main categories of presentation of CDP are:

1. Radiculopathy
2. Myelopathy
3. Radiculomyelopathy
4. Axial neck pain only
5. Symptoms appears in clusters: Cord syndromes.

• Based on the above categories, this patient falls into the radiculomyelopathy category.

 

• Q2: Based on the shown MRI, which nerve root is expected to be compressed?
• The C7 nerve root is the one expected to be affected.

 

• Q3: What is the difference between prefixed and postfixed brachial plexus? How can this difference influence the patient’s brachialgia?
• The brachial plexus roots range from C5 to T1 nerve roots. Sometimes, it can be prefixed, meaning it includes roots from C4 to C8, or postfixed, including roots from C6 to T2. This anatomical variation can influence the patient’s brachialgia due to shifts and aberrations in the spinal cord segments. In a prefixed configuration, a C6-C7 disc prolapse can cause brachialgia in C8 instead of the C7 nerve root. In a postfixed configuration, the same disc prolapse can cause C6 brachialgia instead of affecting the C6 nerve root directly.

 

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Case 2 Chiari malformation type 2 (CM-II)

Figure 2: MRI axial T1.

Clinical presentation

• A male baby who is 35 days old and born full term, the fourth child from a non-consanguineous marriage delivered by C-section.
• The condition began one week after surgery to repair meningocele on January 14, 2024, at Al-Hussein University Hospital.
• The patient has shown progressive increase in head circumference, as indicated by a CT scan revealing hydrocephalus changes.
• Upon examination, the baby is conscious with spontaneous eye movement, a good cry, strong suckling power, and freely moving limbs. The anterior fontanelle measures 2×2 finger breadth and appears tense and bulging, while the head circumference measures 38 cm.

 

• Q1: What is the optimal time for repair of meningomyelocele in Chiari type 2?
• Early closure of the meningomyelocele (MM) defect is not associated with improvement in neurological function, but evidence supports a lower infection rate with early closure. The MM should be closed within 24 hours, regardless of whether the membrane is intact (after 36 hours, the back lesion becomes colonized, increasing the risk of postoperative infection).

 

• Q2: What percentage of patients with MM will develop hydrocephalus HCP?
• Hydrocephalus develops in 65-85% of patients with meningomyelocele (MM). Over 80% of MM patients who will develop hydrocephalus do so before age 6 months. Closure of the MM defect may convert latent hydrocephalus to active hydrocephalus by eliminating a route for cerebrospinal fluid (CSF) drainage, potentially leading to issues like CSF leakage from the wound site of the MM.

 

• Q3: What is the underlying embryology behind the development of meningomyelocele (MM)?
• It is due to failure of closure of the neural tube, specifically the posterior neuropore, which typically closes around 26 days after conception. There are several risk factors associated with this condition; certain drugs, such as Na valproate used for seizures, are implicated. Another significant factor is folic acid deficiency. Therefore, folic acid supplementation should be recommended to all couples planning to have a baby and should ideally be started before conception.

 

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Case 3 Convexity meningioma

Figure 3.1: MRI of the patient:: Coronal sagittal and axial with contrast

Clinical presentation

• Male patient 77 years old.
• The condition began one year ago with recurrent attacks of mild, diffuse, dull aching headaches that worsened over the last two months, accompanied by a history of fainting attacks.
• Two weeks ago, the patient developed an attack of generalized tonic-clonic (GTC) fits lasting about 15 minutes, followed by a postictal state.
• Examination seems to be normal

 

• Q1: Why do meningiomas enhance vividly?
• This is due to its vascularity and the histological features of its cells, which readily accept contrast. However, the most significant factor is its location outside the blood-brain barrier, as the blood-brain barrier typically rejects contrast material, while in the dura, there is no blood-brain barrier.

 

• Q2: How can you differentiate between falcine, parasagittal, and convexity meningiomas when they are in close proximity to the midline?
• This can be done by following the brain mantle in close proximity to the midline. There will be a rim of brain between the parasagittal and convexity meningioma in the coronal plane, and a rim of brain between the falx and parasagittal sinus in the coronal plane. However, sometimes differentiation is only possible intraoperatively. It is worth mentioning that MRV (Magnetic Resonance Venography) may be valuable in assessing differentiation when it shows obliteration of the superior sagittal sinus.

Figure 3.2: differentiation of meningioma in relation to the sinus.

 

 

• Q3: What is the most common microscopic histological feature of meningioma? How can this affect your surgery?
• The most common types are the meningothelial, fibroblastic, and transitional, which share features of both. This can affect the surgery by influencing the consistency of the tumor, which may require the use of CUSA (Cavitron Ultrasonic Surgical Aspirator) or a tissue deprider, or the need for a silk suture technique in the case of a fibroblastic convexity type meningioma.

 

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Case 4 Meningioma En-plaque

Figure 4.1: MRI of the patient: Axial T1, Axial T2 and FLAIR.

Clinical presentation

• Female patient, 48 years old.
• The condition started 7 years ago when the patient developed right eye proptosis.
• 1 year ago, proptosis progressed and was associated with unilateral diminution of vision in the right eye.
• Fundus: Bilateral pale optic discs.
• The proptosis is not pulsatile and no bruit is heard.

 

• Q1: What is the characteristic feature of sphenoorbital meningioma?
• It is characterized by hyperostosis involving the sphenoid bone, pterion, orbital wall, zygomatic bone, temporal bone, and middle cranial fossa, leading to bone thickening that may compress orbital structures. Typically, patients present with proptosis, as shown in this case. Moreover, it is sometimes associated with a sheet of soft meningioma tissue, which may be located in the orbit or the temporal lobe.

 

• Q2: What is the cause of the diminution of vision in this patient?
• It may be due to soft tissue swelling in the orbit, which compresses the optic nerve or affects its blood supply. Moreover, it may be due to narrowing of the optic canal, which can be appreciated on a multi-slice CT scan with a bone window. In this case, decompression of the optic nerve is an essential step in the surgical procedure.

Figure 4.2: CT of the orbit to the patient.

Figure 4.3: Different extension of meningioma in relation to the sphenoid wing.

• The classic triad of sphenoid (spheno-orbital) wing meningioma includes painless proptosis, visual impairment, and ocular paresis. Headache is also a common manifestation, and patients may sometimes experience ptosis. Additionally, patients may present with retro-orbital pain or a sensation of pressure.

 

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Case 5 Lumbar disc prolapse

Figure 5.1: MRI axial T2 of the patient.

Clinical presentation

• Male patient 63 years old.
• The condition started 4 years ago after several instances of lifting heavy weights.
• The patient developed gradual progressive low back pain, which worsened 2 months ago, associated with bilateral sciatica of L5-S1.
• The symptoms include bilateral calf muscle claudication.
• Despite this, the patient retains full power, has intact sensations and sphincters, positive right SLR at 60 degrees, and positive bilateral Patrick’s test.

 

• Q1: What are the different zones of lumbar disc prolapse? Is there any influence of the zone prolapsed on the radiculopathy developed?
• It may be central, subarticular, foraminal, extraforaminal and anterior. A point of differentiation is that foraminal and extraforaminal prolapses will compress the nerve root at the same level as the vertebra above, unlike central and subarticular prolapses, which will compress the traversing root below.

Figure 5.2: Different zones of lumbar disc prolapse.

 

 

• Q2: What is the content of the keyhole configuration in this MRI? And what is the cause of the hyperintensity around these structures?
• The contents of the intervertebral foramen include the nerve root sleeve and segmental intervertebral vessels. The cause of hyperintensity on MRI is due to the fat content.

 

• Q3: How can you differentiate clinically between sciatica due to lumbar disc prolapse and claudication pain caused by lateral recess stenosis?
• This can be differentiated clinically by the following:

1. Pain from lateral recess stenosis increases with standing and walking, similar to claudication pain caused by lumbar canal stenosis, and improves by leaning forward, squatting, or sitting.
2. The Valsalva maneuver can increase pain in cases of lumbar disc prolapse, but not in lateral recess stenosis.
3. The Straight Leg Raise (SLR) test may be positive in lumbar disc prolapse, and pain increases with sitting, unlike lateral recess stenosis, which worsens with prolonged sitting.

 

• Q4: At what degree is the Straight Leg Raise (SLR) considered positive and significant? If a patient has significant SLR limitation on one side, can this patient sit?
• The Straight Leg Raise (SLR) is considered positive if pain develops at 60-70 degrees. Patients with a positive SLR can sit because the SLR test requires unilateral flexion of the hip and extension of the knee to provoke pain, whereas sitting involves bilateral flexion of both the hips and knees.
• Q5: What are the boundaries of the lateral recess? Providing an image would be helpful.
• The boundaries of the lateral recess are:

1. Medially: The medial boundary is formed by the posterior edge of the vertebral body and the intervertebral disc.
2. Laterally: The lateral boundary is created by the pedicle of the vertebral arch.
3. Superiorly: The superior boundary is the inferior aspect of the pedicle above.
4. Inferiorly: The inferior boundary is the superior aspect of the pedicle below.

Figure 5.3: boundaries of the lateral recess.

 

 

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Case 6 Oligodendroglioma

Figure 6.1: MRI of the patient axial T2.

Clinical presentation

• A 36-year-old female patient, medically free, presented with a headache accompanied by blurring of vision, memory affection, and personality changes over the past two months, without any association with vomiting or loss of consciousness.
• She has a history of a single attack of fits two months ago.
• Fundus examination showed grade 1-2 papilledema. Cranial nerves were intact, speech was normal, and she had full power.
• After operation, pathology revealed oligodendroglioma.

 

• Q1: Can you quantify the degree of mass effect in this case?
• Mass effect in this case includes effaced sulci, compressed ventricles, midline shift, and compression of basal cisterns. We can observe compression of the cerebral peduncle by the uncus, which is the most medial part of the temporal lobe. In acute events, such as those seen with acute extradural hemorrhage, this leads to oculomotor nerve palsy, characterized by ipsilateral pupil dilatation and contralateral hemiparesis.

 

• Q2: What possible complications must be counseled preoperatively?
• As the lesion is located in the left dominant post-temporal and parietal Wernicke’s area, there may be an impact on language functions. Therefore, potential language impairment should be discussed with the patient preoperatively.

 

• Q3: What are the major tracts to be considered during surgery in the temporal lobe?

Figure 6.2. Fascicular trajectories are based on Catani and Thiebaut de Schotten (2008), Rilling et al. (2008), Saur et al. (2008), Frey et al. (2008), Makris et al. (2009), and Turken and Dronkers (2011). AF, arcuate fasciculus; CB, cingulum bundle; IFOF, inferior fronto-occipital fasciculus; ILF, inferior longitudinal fasciculus; MLF, middle longitudinal fasciculus; UF, uncinate fasciculus; VP, ventral pathway.

 

 

Q4: Based on pathology, what genetic alteration may affect the prognosis of oligodendroglioma?

• The presence of a 1p19q co-deletion affects the prognosis of oligodendroglioma positively. Patients with this genetic marker typically respond better to chemotherapy and have improved survival rates. Additionally, several surgical and radiological factors can enhance prognosis, including:

1. Younger age at presentation.

2. Frontal lobe location of the tumor.

3. Presence of calcification within the tumor.

4. Reduced degree of enhancement on imaging studies.

5. Smaller size of the lesion, less than 4 cm³.

6. More extensive surgical resection of the tumor.

 

 

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Case 8 Sphenoid wing meningioma

Figure 8.1: MRI of the patient axial T1 with contrast and sagittal with contrast.

Clinical presentation

• A 70-year-old female patient presented to the ER with a decreased level of consciousness (DCL) from two days ago, initially having a Glasgow Coma Scale (GCS) score of 12/15 upon admission. After dehydrating measures, her GCS improved to 14/15. •
• History of Demnetia and Recent memory loss from 1 year
• Additionally, she has a history of headache and blurring of vision dating back three months and experienced a generalized tonic-clonic seizure one year ago.
• Fundoscopic examination showed right-sided papilledema grade 2 and left-sided papilledema grade 3.

 

• Q1: What are the grades of papilledema?

Figure 8.2: Grades of papilledema.

 

 

• Q2: What are the different types of globoid meningioma based on the sphenoid wing?

Figure 8.3: (a) Art illustration of the different anatomical segments of the sphenoid wing. (b) MRI T1 with gadolinium axial (top) and coronal (bottom) views showing the surgical types of sphenoid wing meningioma. https://link.springer.com/chapter/10.1007/978-3-030-99321-4_17/figures/9

 

 

• Q3: What is the classification of clinoidal meningioma?
• Type I clinoidal meningiomas are believed to originate from the subclinoidal dura at the most proximal intradural entry point of the internal carotid artery, just before it enters the arachnoidal cisternal space. Al-Mefty noted that these tumors are extraarachnoidal, making them more adherent to the internal carotid artery and difficult to surgically remove, often resulting in higher rates of subtotal resection and recurrence.
• Type II clinoidal meningiomas are thought to arise from the superolateral aspect of the anterior clinoid process. As these tumors grow, they are enveloped by the arachnoid layers around the carotid cistern, which prevents significant adherence of the tumor to the adventitia of the internal carotid artery wall, facilitating easier surgical dissection and more complete resections.
• Type III clinoidal meningiomas originate from the region of the optic foramen and extend into the optic canal. Due to their growth pattern within the optic canal region, these tumors tend to become symptomatic early and are diagnosed at smaller sizes compared to Types I and II.

Figure 8.4: (Bony anatomy of the anterior clinoid process region. (Left) The course of the optic nerve (straight arrow) and the course of the internal carotid artery (curved arrow). OC, optic canal; ACP, anterior clinoid process; PCP, posterior clinoid process. (Right) The origin of the different types of clinoidal meningiomas.

 

 

• Q4 : How can the location of a sphenoid wing meningioma affect the clinical presentation of the patient?
• Depending on the location, the lateral type of sphenoid wing meningioma can present with irritative symptoms such as fits. The middle type can present with temporal lobe epilepsy or frontal symptoms due to subfrontal extension, while the medial type is typically presented by visual symptoms due to compression of the optic nerve. In the case presented, the patient’s symptoms coincide with the middle type. The bilateral presentation of papilledema is due to the mass effect, which increases the intracranial pressure.

 

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Case 9 Lumbar canal stenosis

Figure 9.1: MRI of the patient axial T2 and sagittal T2.

Clinical presentation

• A 68-year-old male patient with diabetes and hypertension presented with right sciatica affecting the L4 and L5 nerve distribution for the past 2.5 years.
• has experienced calf muscle claudication for one year.

 

• Q1: What is the pathophysiology of neurogenic claudication?
• The pathophysiology of neurogenic claudication includes the following factors:

1. Direct compression on the nerve roots from osteophytes or hypertrophy of the ligamentum flavum, especially if superimposed on congenital spinal canal stenosis.

2. Ischemia and venous congestion due to compression of segmental vessels and epidural veins.

3. Repeated local trauma from repetitive movements.

 

 

• Q2: Given the patient’s diabetes and advanced age, is there concern for other diseases that may manifest as claudication, considering the risk factors of diabetes and old age?
• Given the patient’s diabetes and advanced age, there is concern that the claudication might also indicate another disease, such as peripheral arterial disease (PAD), commonly associated with these risk factors. This condition often presents with claudication, characterized by pain and cramping in the legs due to reduced blood flow. Assessment of peripheral vascularity should include observing trophic changes in the lower limbs, checking pulsations, and conducting duplex ultrasound and angiography to evaluate the vascularity of the lower limbs.

 

• Q3: What are the minimally invasive operations that can be performed for lumbar canal stenosis?
• It includes the following:

1. Bilateral laminoforaminotomy.

2. Unilateral laminoforaminotomy and contralateral decompression from the same side.

3. X-Stop implant.

4. Epidural steroid injection and radiofrequency.

Figure 9.2: X-stop.

 

 

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Case 10 Chiari malformation type 1 (CM-I)

Figure 10.1: MRI of the patient Pre and post operative.

Clinical presentation

• A 39-year-old female patient presented with neck pain and weakness and atrophy in both hands (more pronounced on the right) for the past 6 months.
• History of suboccipital headaches dating back 2 years.
• Noted weakness and atrophy in hands starting 4 months ago.
• Lower Limbs: Full power
• Upper Limbs: Right—shoulder, elbow G4; hand G3. Left—shoulder, elbow full power; hand G4.
• Hyperreflexia in the lower limbs.

 

• Q1: Can you describe the pathology seen in the MRI?

Sagittal T1 and T2-weighted image findings:

• The cervical curvature is straightened with good vertebral alignment. There is no vertebral structural collapse or marrow signal alteration.
• The tonsils are pointed and peg-tailed, with tonsillar descent to the level of the C1 arch. There is an oval cyst at the beginning of the cord, accompanied by hyperintensity extending throughout the cervical cord and downwards, representing syringomyelia.

 

• Q2: What is the aim of surgery in the case of Chiari 1 malformation?
• The aim of surgery in the case of Chiari 1 malformation is to enlarge the posterior fossa and reestablish the flow of cerebrospinal fluid (CSF) between the cranial and spinal compartments. This can be achieved through multiple techniques ranging from simple bony decompression, which ensures CSF flow as verified by ultrasound, to more extensive procedures involving arachnoid lysis, tonsillar coagulation, and duroplasty.

Figure 10.2: diagrammatic represent explanation of syringomyelic symptoms.

• Pain : Dysthetic pain without dermatomal distribution.
• Motor : syringomyelic syndrome : segmental weakness, decrease tendon jerk, dissociated sensory loss.
• Sensory : Cape distribution , Dissociated ( loss of pain and temp with preserved light touch ) ,Gloves and stocking , may predispose to trophic ulcers
• Miscellaneous : Horner’s in cervical ,Scoliosis and torticollis.

 

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Case 11 High Grade glioma

Figure 11-1: MRI brain of the patient: A coronal with contrast, B sagittal with contrast, C T2 axial image, D axial with contrast.

Clinical presentation

• Male patient 37 years old with history of progressive weakness with recurrent attacks of parasthesia.
• Recurrent attacks of GTCs 1 month ago.
• Left side weakness grade 4/5.

 

• Q1: Describe MRI finding?
• The MRI reveals a right deep frontal non-homogeneous lesion compressing and invading the corpus callosum, with surrounding edema extending into the adjacent parietal lobe.

 

• Q2: What is the differential diagnosis of ring enhancing lesion?
• (MAGIC DR) mnemonic. M – Metastasis A – Abscess G – Glioblastoma multiforme I – Infarct (subacute phase) C – Contusion D – Demyelinating disease (eg. tumefactive MS) R – Radiation necrosis.
• Malignant astrocytoma, metastases, abscess including toxoplasmosis, lymphomas, resolving hematoma, cysticercosis cyst, trauma and infarction.
• Abscess

Ring enhancement is typically thinner than that seen in glioblastoma multiforme (GBM), with a T2 hypointense rim and typical diffusion restriction. Magnetic resonance spectroscopy (MRS) may show metabolites such as succinate and amino acids.

• Metastasis

Typically, there are multiple lesions at gray-white junctions. The lesions are more often round than infiltrating. The primary tumor is often known, although a single lesion may be indistinguishable.

• Primary CNS lymphoma

Periventricular enhancing mass, often crossing the corpus callosum, typically appears isointense or hypointense on T2-weighted images.

 

 

• Q3: What is the new WHO classification of adult-type diffuse glioma?
• The recent WHO classification 5^th edition classifies it into:

Astrocytoma, IDH mutant

astrocytoma, IDH-mutant, grade 2

astrocytoma, IDH-mutant, grade 3

astrocytoma, IDH-mutant, grade 4

Oligodendroglioma, IDH-mutant & 1p/19q codeleted

oligodendroglioma, IDH-mutant & 1p/19q codeleted, grade 2

oligodendroglioma, IDH-mutant & 1p/19q codeleted, grade 3

Glioblastoma, IDH-wildtype 4

giant cell glioblastoma G 4

gliosarcoma G 4

epithelioid glioblastoma G 4

 

 

• Q4: Does age have any prognostic factor in glioblastoma?

Yes, GBM occur in 2 forms and two age group:

• Denovo type, occur in old age with bad prognosis.
• 2ndry type, occur in younger age as a result of differentiation of low-grade type, with better prognosis.

 

• Q5: How does high grade glioma appear in angiography?
• Tumour blush with early draining vein.

 

• Q6: When do you consider Metastatic work up in a suspected case of high-grade glioma?

In the following situations:

• Multiple brain lesions.
• History of cancer.
• Single ring enhancing lesion at gray-white interface.
• Posterior fossa cerebellar lesion in adults.

 

• Q7: What is the pathological basis of the different patterns of enhancement in different grades of glioma?
• The principle involves the degree of destruction of the blood-brain barrier; the greater the destruction, the more pronounced the enhancement. In grade 2, there is no enhancement; in grade 3, there is patchy enhancement; in grade 4, there is solid enhancement; and in glioblastoma multiforme (GBM), there is necrosis with irregular ring enhancement due to rapid growth.

 

• Q8: What is the general role of surgery in high grade glioma?
• Maximal gross safe resection, when possible, followed by chemotherapy with radiation.

 

• Q9: What is the advantage of surgery and gross total resection?
• It helps in:

1. Obtain generous tissue for diagnosis.
2. Reduce tumour burden which facilitates adjuvant therapy.
3. Reduce mass effect and improve function.
4. Decrease ICP and decrease oedema.
5. Reduce seizure frequency.
6. Decrease the risk of wounded glioma (hemorrhage and oedema).
7. Increase time to tumour progression and increase median survival.

 

• Q10: What is the relative contraindication for surgery (meaning consideration for a biopsy)?
• It includes the following:

1. Extensive dominant lobe high grade glioma
2. Elderly, patient older than 75 years.
3. KPS less than 70
4. Patient with poor medical condition
5. Multicentric glioma
6. Lesions with bilateral involvement (butterfly glioma), except surgery are indicated to decrease ICP and risk of herniation.

 

• Q11: As regards this case with relation to the motor strip, what are methods help in localization and assist in maximal gross safe resection?
• We can use the following methods:

1. MRI anatomy and surrounding sulcal landmarks.
2. Functional MRI.
3. Neuro-navigator.
4. Intraoperative MRI.
5. Intraoperative mapping and brain stimulation either:
6. A wake craniotomy with mapping.
7. Under general anesthesia with SSEPs and MUPs and neuromonitoring.

Figure11-2: intraoperative skull-scalp metric points A, dotted line for sagittal suture, B, Pre-central sulcus, C, coronal suture, D, Central sulcus, E, superior frontal sulcus, F, and its arrow, referred to staphenion which is the meeting of superior temporal line and coronal suture. The dotted circle outlines the lesion on the cortex.

 

 

• Q12: What is the expected semiology of a lesion in this location?
• The lesion is in the white matter tracts serving the motor strip of the upper and lower limb with adjacent oedema in the sensory area, weakness and sensory affection will be the predominant symptoms.

 

• Q13: What is the stupp protocol for adjuvant therapy for high grade glioma?
• After surgery, adjuvant radiotherapy is administered for 4 weeks, followed by chemotherapy with temozolomide (an oral alkylating agent that destroys DNA) for 6 cycles, with 5 days per month for 6 months.

 

• Q14: What is the role of the MGMT promoter gene in the prognosis of high-grade glioma?
• MGMT is a DNA-repair enzyme that counters the effects of chemotherapy in gliomas, leading to shorter survival. The MGMT promoter gene is responsible for the production of the MGMT enzyme. High MGMT activity is associated with shorter survival. Methylation of the MGMT promoter gene leads to decreased activity of the MGMT enzyme, which improves survival outcomes.

 

• Q15: What are the good prognostic factors for high grade glioma?
• It includes:

1. Younger age less than 40 years.
2. Decrease activity of MGMT
3. Pre-operative KPS more than 80.
4. Site of the lesion, frontal lobe is better.
5. Extent of resection, more than 90% is better.
6. Degree of enhancement, lower enhancement is better.
7. Size of lesion, tumour less than 6cm3 is better.
8. Histological grading, lower grades are better.

 

• Q16: What is the Gliadel wafer?
• It is an implant loaded with chemotherapy applied to the resection cavity after tumour excision. The principle is to bypass the blood brain barrier and to increase concentration of chemotherapy. Its complications are seizure and infection.

 

• Q17: What is the usual site of recurrence of high-grade glioma? When to re-operate a recurrent high-grade glioma? What is the benefit of re-surgery?
• 90% of recurrence occurs at the site of same site of original tumour, and 10% occur at remote site due to spread through white matter tracts and commissures.
• Indication of re-surgery:

1. Younger age.
2. KPS more than 70.
3. Long time between initial surgery and recurrence.
4. Histological lower grade at the initial surgery.

• Re-surgery increases survival by 9 months in GBM and 22 months in grade 3.

 

• Q18: What is the difference between multi-centric and multi-focal glioma? What is meningeal gliomatosis? What is the goal of treatment in these gliomas?
• The term multi-centric and multi-focal glioma is used to describe multiple gliomas, with the difference that, multi-focal glioma is due to tract spread such as fronto-temporal glioma connected through uncinate fasciculus, however in multi-centric glioma, the gliomas is not connected to each other such gliomas occur in NF1 and tuberous sclerosis.
• The term meningeal gliomatosis refers to CSF distant spread of GBM (CSF Mets).
• The goal of treatment in these types is brain radiation and chemotherapy, with surgery considered only for life threatening herniation or functional deterioration due to mass effect.

 

• Q19: What is meant by pseudo progression?
• It is a term referred to progressive increase in contrast enhanced area on MRI following completion of Stupp protocol which mimic tumour recurrence. It usually appears within 3 months after completion of radiation in 30-60% of patients and should be considered in the differential diagnosis of tumour recurrence. It occurs due to radiation necrosis caused by endothelial injury and destruction of BBB.

 

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Case 12 Recurrent lumbar disc prolapse

Figure 12.1: MRI of the patient sagittal T2.

 

 

• Q1: Which root is affected in an L4-5-disc herniation?
• A posterolateral L4-L5 disc herniation affects the L5 nerve root, while a far-lateral herniation affects the L4 nerve root.

 

• Q2: Why are symptoms and signs more severe in recurrent cases than in de novo ones, even with smaller-sized discs?
• This is because fibrosis and adhesions developed after the first surgery restricts the movement of the nerve root, making it more vulnerable to compression.

 

• Q3: What is the percentage of failed back syndrome after lumbar operations?
• It’s difficult to calculate percentage accurately but it’s about 30%.

 

• Q4: What are the Causes of post op failed back syndrome?

It includes:

• Inadequate decompression (mostly residual lateral recess stenosis)
• Aggressive decompression (compromising spinal stability)
• Patient selection (work claimers mostly and psychotic patients)
• Deficient decision (neglected instability)
• Recurrent disc Thecal and roots scarring
• What is pelvic incidence (PI)?
• The angle is measured between two lines: the first from the center of the femoral head to the middle of the upper S1 plate, and the second a perpendicular line to the upper S1 plate. This value is unchangeable and specific to each patient. It helps in the correction of abnormal lumbar lordosis. A PI-LL (pelvic incidence minus lumbar lordosis) greater than 11 degrees indicates mismatching and correlates with the patient’s axial symptoms. It is also the sum of the sacral slope and pelvic tilt. All these measurements are taken in the sagittal plane.

Figure 12.1: sacral slope and pelvic incidence.

 

 

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Case 13 Olfactory groove meningioma

Figure 13: MRI of the patient axial with contrast.

Clinical presentation

• A 62-year-old male patient presented with a condition that started four months ago with a fainting attack, followed by the development of dizziness two months later.
• The condition is associated with a diffuse, dull, aching headache that increases with stress and decreases with analgesics, not associated with vomiting.
• Fundus examination showed no papilledema.
• Motor functions are at full power.
• Sensory functions and sphincters are intact.

 

• Q1 : Could you tell the sequence of the MRI shown here? What clues lead you to your answer?
• It is a T1 with contrast, as the sinuses are enhancing. Venous sinus enhancement is important when evaluating contrast patterns of enhancement because it serves as a guide that the MRI was taken under optimal conditions.

 

• Q2: From the appearance of the lesion, what is its origin (both anatomical and pathological/microscopic)? What is the main blood supply to this extra-axial lesion?
• Anatomically, the lesion originates from the cribriform plate. Pathologically, it involves arachnoid cap cells. The main blood supply to the lesion is from the ethmoidal artery, which arises from the ophthalmic artery.

 

• Q3: During surgery for this lesion, what is the most critical area on the surface of the tumor related to important structures, and what are these important structures?
• The most critical surface is the postero-superior surface. It is located near important structures such as the anterior cerebral artery, optic nerve and chiasm, and the pituitary stalk. Sharp dissection is required in this area during surgery.

 

 

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Case 14 Spinal Metastasis

Figure 14.1: MRI and CT of the patient: A CT sagittal spine, B MRI T2, C T1 with and without contrast, D Axial with contrast.

Clinical presentation

• Female patient 48 years with 3 months history of ago neck pain associated with Bilateral brachialgia of diffuse dermatomal distribution more on the left upper limb.
• 3wks ago pt developed left UL weakness followed by Right UL weakness more at hands within the last 3 weeks.
• There is a history rectal carcinoma excision followed by radiotherapy and chemotherapy in the previous year.
• On examination there is bilateral finger drop with weakness in finger extension grade 1/5 and 2/5 on the right and left respectively, otherwise patient is full power.

 

• Q1: What are the main movements of the upper limb with root value and nerve supply?

Movement	Nerve root	Peripheral nerve
Shoulder abduction	C5	Axillary
Elbow flexion	C5-6	Musculocutaneous
Elbow extension	C6-7	Radial
Wrist extension	C6-7	Radial
Wrist flexion	C7-8	Median
Finger flexion	C8	Median
Finger extension	C8	Radial
Finger abduction	C8	Ulnar

 

• Q2: What is the differential diagnosis of the radiological finding?
• It includes the following:

1. Osteoporosis
2. Neoplastic lesion (Metastasis, and 1ry bone tumours)
3. Infection
4. Chronic renal failure
5. Avascular necrosis of the vertebral body (with steroid use)
6. Vertebrae plana

 

• Q3: What is the NOMS algorithm for spinal metastasis?

 

 

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Case 15 Skull lesion

Figure 15: MRI and CT of the patient: A coronal with contrast, B axial T2, C sagittal T1, D CT brain.

Clinical presentation

• A 26-year-old male patient with a history of progressive non-pulsatile proptosis associated with diminished vision.
• He has recurrent attacks of left frontal and retroorbital headaches that do not respond to medication.
• Fundus examination reveals no abnormalities.

 

• Q1: Describe the MRI finding?
• The imaging reveals an anterior skull base lesion eroding the right orbital roof and cribriform plate, with extension into the orbit and nose. It is surrounded by a shell of calcification, featuring mixed internal intensity and heterogeneous enhancement.

 

• Q2: What is your differential diagnosis?

It includes:

• Fibrous dysplasia
• Fibro-osseous tumors (e.g., ossifying fibroma)
• Primary bone tumors
• Nasopharyngeal tumor
• Skull base meningioma
• Hemangiopericytoma
• Metastasis
• Other less likely diagnoses include lymphoma, osteosarcoma, Paget’s disease, Langerhans cell histiocytosis, infection (osteomyelitis, soft tissue infection, etc.), and aneurysmal bone cyst.

 

• Q3: How can you differentiate between mechanical diplopia caused by an abnormal mass compressing the eye and neurological diplopia due to oculomotor nerve palsy?
• This can be differentiated by measuring the intraocular pressure while the patient tries to look in the direction of the limited gaze. In cases of neurological diplopia, the intraocular pressure will remain normal.

 

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Case 16 Spondylolithesis

Figure 16.1: MRI sagittal T2 and x ray of the patient

 

 

• Q1: According to the Meyerding classification, which grade of spondylolisthesis is shown on this lateral radiograph of the lumbar spine?
• Grade 2

Figure 16.2: Meyerding classification.

• Q2: Degenerative spondylolisthesis is typically caused by: –

1. Degenerative facet arthrosis.
2. Disc degeneration.
3. Pars interarticularis remodeling.
4. Trauma.

• The correct answer is Degenerative facet arthrosis.

 

• Q3: What type of Modic changes are present here, and what are signal characteristics on MRI of the lumbar spine?
• Modic type 1 (bone marrow oedema)

Figure 16.3: Modic changes.

 

 

• Q4: During surgery to this case which the nerve root needs to be decompressed?
• The nerve roots of concern to be decompressed are the L4 and L5 roots. This differs from lumbar disc prolapse, where L4 is usually compressed by the slippage of the vertebrae, unlike lumbar disc prolapse, which typically compresses L5 away from the L4 foramen. Intraoperatively and after decompression, bilateral L4 and bilateral L5 roots need to be checked.

 

• Q5: During transpedicular screw application, what is the direction of the screw insertion? Which structures are strong?
• It is either aligned with the longitudinal direction of the pedicle or directed towards the superior end plate. The latter is preferable as it is stouter due to the stronger bone near the end plate.

 

 

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Case 17 Multiple brain lesions

Figure 17: MRI T1 with contrast.

Clinical presentation

• Male patient 63 years with 3 months the condition has started 2 months ago with recurrent attacks of mild diffuse dull aching headache, dizziness & generalized fatigue aggravated 10 days ago with DCL and speech difficulty.

 

• Q1: Which of the following tumors is most likely to have prominent flow voids?

1. Cerebral metastasis.
2. Glioblastoma.
3. Hemangioblastoma.
4. Medulloblastoma.
5. Pilocytic astrocytoma.

• Hemangioblastoma

 

• Q2: What percentage of cerebral metastases are solitary at the time of presentation?

1. 5%
2. 25%
3. 50%
4. 75%
5. 95%

• 25%

 

• Q3: Which of the following is most likely to metastasize to the brain?

1. Breast cancer.
2. Colorectal carcinoma.
3. Lung cancer.
4. Malignant melanoma.
5. Renal cell carcinoma.

• Lung cancer
• Within 2 years, 80% of patients who survive lung cancer will develop brain metastasis.

 

• Q4: What are the factors determining prognosis in a patient with cerebral metastases?

It includes:

• Karnofsky Performance Status (KPS) is the most important factor; breast cancer responds well.
• Specific primary tumor type and its response to chemotherapy and radiotherapy.
• State of systemic disease.
• Length of time since the diagnosis of the primary tumor; a longer duration is associated with a better prognosis.
• Size and location of brain metastases, with worse outcomes in the posterior fossa.
• Age: older than 60 years is associated with a worse prognosis compared to younger patients.
• The number of metastases is also a prognostic factor.
• Female gender tends to have a better prognosis than males.

 

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Case 18 Lumbar canal stenosis

Figure 18.1: MRI sagittal T2.

 

 

• Q1: What’s the embryological origin of the nucleus pulposus?
• The embryological origin of the nucleus pulposus is the primitive notochord.

 

• Q2: What’s the type of collagen in the nucleus pulposus and annulus fibrosus?
• The annulus fibrosus contains collagen type 1, while the nucleus pulposus contains collagen types 2 and 3.

 

• Q3: Describe the motor affection of the L5 nerve root?
• L5 nerve root affection primarily causes weakness in the extensor hallucis longus.

 

• Q4: provide diagrammatic picture for lumbar back muscles?

Figure 18-2: back muscle.

• Q5: What is sino-vertebral nerve?
• Sino-vertebral nerve is a sensory nerve that innervates the inter vertebral disc, ligament, annulus, and periosteum of spinal canal. It is considered recurrent nerve from the ventral ramus of spinal root reentering the intervertebral foramina to innervate the previous structures.

 

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Case 19 Aqueductal stenosis

Figure 19: MRI axial T1.

 

 

• Q1: What is the score used to determine the ETV success rate, and what are the items it considers?
• The score (0-90) for predicting the success of an ETV depends on three factors: age, etiology, and history of VP shunt insertion. It is more likely to succeed in patients aged 2 years or older. Success is more likely when the etiology is obstruction rather than infection. A previous VP shunt decreases the chances of success.

 

• Q2: Why does the success rate increase with the patient’s age?
• The success rate increases with age due to the patency of the prepontine cistern.

 

• Q3: What methods are used to perforate the floor of the third ventricle, and which is the safest?
• The safest method to perforate the floor of the third ventricle is using a Fogarty catheter. Monopolar cautery or grasping forceps can also be used.

 

• Q4 What are the causes of aqueductal stenosis?
• Congenital Causes:

1. Aqueductal Gliosis: This involves the proliferation of glial cells within the aqueduct, leading to its narrowing.
2. Aqueductal Webs or Septa: Thin membranous structures can form within the aqueduct, partially or completely obstructing it.
3. Congenital Stenosis: Some individuals may be born with a naturally narrow aqueduct due to developmental anomalies.

• Acquired Causes:

1. Infections: Infections like meningitis can lead to inflammation and subsequent scarring, narrowing the aqueduct.
2. Hemorrhage: Bleeding in or around the aqueduct can cause clots and fibrotic changes, leading to stenosis.
3. Neoplasms: Tumors within or near the aqueduct can compress it and cause obstruction.
4. Trauma: Head injuries can result in swelling and scarring, affecting the aqueduct.

• Idiopathic Causes:

In some cases, the cause of aqueductal stenosis cannot be determined and is labeled idiopathic.

 

 

 

 

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Case 20 CPA schwannoma

Figure 20: sagittal and coronal with contrast.

 

 

• Q1: D.D. of CPA lesions?
• Vestibular schwannoma is the most common followed by meningioma, Epidermoid.

 

• Q2: Which of the following is the most common tumor of the cerebellopontine angle?
  1. Arachnoid cyst.
  2. Epidermoid cyst.
  3. Facial nerve schwannoma.
  4. Meningioma.
  5. Trigeminal schwannoma.
  6. Vestibular schwannoma.
• Vestibular schwannoma.

 

• Q3: All the following features are those of vestibular schwannoma EXCEPT: –

1. Extension to the Meckel cave.
2. “Ice cream cone” appearance.
3. Intracanalicular component.
4. May have cystic components.
5. Widening the porus acusticus.

• Extension to the Meckel cave.

 

• Q4: Which of these is NOT a recognized cause of pulsatile tinnitus?
  1. Aberrant internal carotid artery.
  2. Idiopathic intracranial hypertension.
  3. Jugular bulb dehiscence.
  4. Sigmoid plate diverticulum.
  5. Vestibular schwannoma.
• Vestibular schwannoma.

 

• Q4: Is facial nerve palsy common in CPA acoustic schwannomas, and what is the cause?
• Facial nerve palsy is uncommon in cases of CPA acoustic schwannomas due to the resilience of motor nerves like the facial nerve, which can accommodate compression and stretching. In contrast, the cochlear nerve, which mediates hearing, is usually affected early due to the sensitive nature of sensory nerves.

 

 

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Case 21 Cervical spondylotic myelopathy

Figure 21: MRI of the patient sagittal T2

 

• Q1:What is that abnormal cord signal and why?
• Extensive abnormal hyperintensity is noted across three levels with a swollen cord at C5-6. There is no reported history of trauma, suggesting potential causes such as spinal cord ischemia, neoplastic involvement, or a demyelinating process. Additionally, there is a posterior disc herniation at C5/6.

 

• Q2:What is the normal lordotic cervical angle?
• Normal lordosis is maintained between 20-35 degrees.

 

• Q3:What is normal cervical canal diameter?
• Mean of normal male cervical canal diameter ranges from 16.5 to 21.4 mm Females 15.5 to 20.2 mm

 

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Case 22 Pituitary macroadenoma

Figure 22-1: MRI of the patient axial with contrat.

 

• Q1. What is Knosp classification?

• Figure 22-2: sinus invasion classification

 

• Q2. What are the Types of sphenoid sinus pneumatization?

Figure 22-3A. Choncal,B. presellar, C.sellar and D.post sellar (types of sphenoid sinus pneumatization )

 

 

• Q3: What is the sequence of tumor removal in this case to achieve maximum tumor resection and avoid CSF leak?
• The usual sequence for pituitary tumor removal is as follows: remove the inferior portion first, then the sides, and finally the superior portion. This sequence aims to avoid obstructing the view with the diaphragm sellae if the superior part is removed first, and it minimizes the likelihood of a CSF leak.

 

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Case 23 Drug Resistant epilepsy (mesial temporal abnormality)

Figure 1-1: MRI brain of the patient axial FLAIR, Coronal T2, Axial T2 and Coronal FLAIR.

Clinical presentation

• Female patient, 12 years old, complains of recurrent attacks of complex partial seizures that started at the age of 2.
• The attacks start with an aura, including sensations of fear and vertigo, followed by staring with no response to conversation. The condition is associated with automatisms such as involuntary purposeless acts like lip-smacking and eye blinking.
• There is no neurological deficit.
• The patient is on Tiratam, Tegretol, Lamictal, and Conviban.
• Ictal EEG shows right frontal spikes that spread to the right hemisphere and then become diffuse.

 

• Q1: What is meant by drug-resistant epilepsy (DRE)? Is a 2-year period mandatory before considering extra-medical intervention?
• Failure of an adequate trial of two tolerated, appropriately chosen, and correctly used anti-epileptic drug (AED) schedules to achieve seizure freedom, typically for 2 years, but there is no lower limit for surgically suitable candidates. This means that when resistance to AEDs occurs in the presence of surgical lesions that coincide with seizures, there is no reason to wait for two years in the case of DRE.

 

• Q2: Could DRE be suspected early in the disease?

It can be suspected if the following occur:

• Low efficacy with the appropriately chosen first drug.
• Ineffective outcome with two appropriate and adequate drugs; a third drug will benefit less than 5%.
• When two drugs fail to adequately control epilepsy, an investigation of refractory epilepsy should be initiated. We are losing neurons; time is neurons.

 

• Q3: What are the findings in the MRI?
• Marked asymmetry of the hippocampal heads with an atrophic right side. Additionally, the right hippocampus demonstrates a high signal on FLAIR. There is also an abnormality in the cortex and white matter architecture in the right temporal lobe compared to the left side, particularly in the anterior part of the temporal lobe.

 

Figure 1-2: Coronal demonstration of the temporal lobe and surrounding structures.

 

Figure 1-3: Axial demonstration of the mesial temporal lobe and surrounding structures.

 

 

• Q4: How can you explain the right frontal spike despite the lesion’s location appearing in the MRI?
• When the origin of the focus is in the mesial temporal lobe, it can pass to the frontal lobe through the uncinate fasciculus. This can be detected in the surface EEG, appearing as if it arises from the frontal lobe, which is not the case. This can be more specifically detected by using a subdural grid or stereotactic EEG. Additionally, interictal hypometabolism can be detected using a PET scan.
•  
• Q5: How is a decision made regarding epilepsy surgery in cases of DRE?

This is a simple way to think:

• Is there a focus?

Yes

• Can it be removed safely?

                Yes: Lesionectomy

                 No: Multiple Subpial Transection (MST)

No: Generalized

• If one hemisphere: Hemispherotomy
• If bilateral

                Corpus Callosotomy

                 Vagal Nerve Stimulation (VNS)

Figure 1-4: How to make a decision in DRE.