MSC Neuro 25 p2

1.Neuroectodermal/glial tumors (56%): Astrocytomas, medulloblastomas, gliomas, pineoblastomas.

2.Meningeal and vascular tumors (20%): Meningiomas, angiomas.

3.Sellar region tumors (11%): Pituitary adenomas, craniopharyngiomas.

4.Bidermal (mixed composition)

5.Heterotopic tumors (epidermoids, dermoids)

6.Systemic tumors (neurofibromatosis, meningiomatosis)

7.Metastatic tumors (lung, breast, pelvis)

8.Tumors growing into cranial cavity (sarcomas)

WHO Grading of Gliomas:

Grade I-II: Low grade, slow-growing; pilocytic astrocytoma common in children.

Grade III-IV: High grade, aggressive; anaplastic astrocytoma, glioblastoma multiforme (GBM).

Etiology

Some brain tumors are hereditary, e.g., neurofibromatosis and cerebellar ganglion tumors (autosomal dominant).

Meningiomas can appear 15-25 years after x-ray exposure.

Trauma linked to vascular tumors' development.

Tumor frequency varies by age: common in early childhood, decreases, then peaks around 50 years, and decreases again in old age.

Pathomorphology and Age-related Distribution

Childhood/adolescence: medulloblastomas, cerebellar astrocytomas, brainstem spongioblastomas, craniopharyngioma, ependymomas.

Ages 20-50: meningiomas, cerebral gliomas, pituitary adenomas.

Above 45: gliomas, meningiomas, acoustic neuromas, metastases.

Over 60: glioblastomas, neurinomas, brain metastases predominate.

Malignant gliomas predominantly in cerebral hemispheres; benign tumors more common in brainstem and cerebellum.

Classification (L.I. Smirnov, 1954)

According to cell maturity:

Surgical excision aiming for maximal tumor removal.

Radiation therapy and chemotherapy, especially in high-grade and unresectable tumors.

Medical management of raised intracranial pressure and symptoms.

Pituitary tumors often require medical therapy (dopamine agonists for prolactinomas) or surgical/endoscopic removal.

39.Shell-vascular tumors of the brain. Treatment.

Shell-Vascular Tumors of the Brain and their Treatment: Summary

Overview

Shell-vascular tumors include primarily meningiomas, which are the most common CNS tumors (~35%).

Origin: arachnoendothelial cells in dura mater, less often from choroid plexus.

Other less common tumors: hemangiopericytoma, fibrous histiocytoma, melanoma, diffuse meningeal sarcomatosis.

Etiology: some hereditary cases (e.g., neurofibromatosis); high prevalence due to genetic and environmental factors like radiation exposure.

Histology & Classification

Meningiomas histologically classified as:

Grade I: typical meningiomas (majority), including meningothelial (~60%), transitional (~25%), fibrous (~12%) types.

Grade II: atypical meningiomas.

Grade III: anaplastic (malignant) meningiomas.

Tend to occur with hyperostosis (bone thickening) due to tumor-stimulated osteoblast activity.

Often well-circumscribed, encapsulated by dura, but some infiltrate locally.

Clinical Features

Manifestations depend on tumor location.

Symptoms include headaches, seizures, focal neurologic deficits.

Tumors near skull base can cause cranial nerve palsies.

Early detection often due to palpable scalp swelling or cranial deformities (hyperostosis).

Treatment

Surgery:

Radical surgical removal is primary treatment.

Resection includes tumor mass, involved dura mater, and affected bone.

Complete removal offers a low recurrence rate (~15% within 15 years).

Radiation therapy:

Adjuvant radiotherapy for atypical/anaplastic or incompletely resected tumors.

Modalities include external beam radiation, stereotactic radiosurgery (e.g., Gamma Knife), fractionated radiotherapy, IMRT, and proton therapy.

Radiation controls tumor growth and reduces recurrence risk.

Observation:

Small, asymptomatic meningiomas with no edema may be monitored with serial MRIs.

Chemotherapy:

Generally ineffective at present; experimental agents under study.

Special Considerations:

Multiple meningiomas require careful individualized management.

40.Tumors of the posterior cranial fossa - neurinomas, meningiomas, gliomas. Care.

Tumors of the Posterior Cranial Fossa:

Common Tumor Types

Neuromas: Mostly vestibular (acoustic) neuromas originating from the vestibular branch of the auditory nerve.

Meningiomas: Arise from the meninges in the posterior fossa.

Gliomas: Tumors of glial origin in the cerebellum, brainstem, and fourth ventricle region.

Clinical Features

Early cerebral symptoms such as diffuse headaches (especially early mornings), nausea, vomiting, and signs of increased intracranial pressure (hypertensivehydrocephalic crises).

Dizziness, nystagmus, and cerebellar signs (impaired coordination on the affected side).

Cranial nerve weakness (especially facial muscles, hearing loss in acoustic neuroma).

Neurological deficits from brainstem compression and hydrocephalus.

Tumors of the cerebellar vermis present with gait disturbances, posture abnormalities.

Diagnostics

Detailed clinical history and neurological exam.

MRI is the imaging of choice for tumor localization, size, and involvement.

CT scan and vertebral angiography can assist but are less informative than MRI.

Treatment

Surgery: Mainstay for most posterior fossa tumors, aiming at maximal safe resection.

Management of Hydrocephalus: Ventricular drainage or endoscopic third ventriculostomy may be required before, during, or after surgery.

Radiation Therapy: Postoperative radiation may be needed for malignant or residual tumors.

Conservative management: For non-progressive or inaccessible tumors, with observation and symptomatic treatment.

41.Pituitary adenomas. Clinic, diagnosis, and treatment.

PituitaryAdenomas: Summary

Clinic:

Tumors of the anterior pituitary lobe, located in the sella turcica.

Present with endocrine disorders (hormone hypersecretion or deficiency) and/or mass effect.

Compression of optic chiasm leads to bitemporal hemianopsia.

Cranial nerve involvement: oculomotor (III), abducens (VI), trigeminal (V) nerves.

Symptoms: visual disturbances, headache, hormonal imbalances.

Types based on cell staining and hormone secretion:

Chromophobic adenoma: results in secondary hypopituitarism, symptoms like sexual dysfunction, obesity, metabolic alterations.

Eosinophilic adenoma: causes acromegaly/gigantism (enlarged hands, feet, facial bones).

Basophilic adenoma: produces Cushing’s disease symptoms (obesity, hypertension, diabetes).

Diagnosis:

Clinical picture: hormone-related symptoms, visual field defects.

Imaging: MRI or CTshowing tumor size, location, bone changes.

Hormonal assays: serum hormone levels (e.g., prolactin,ACTH, GH).

Radiologic studies may show enlargement/destruction of sella turcica. Treatment:

Observation: for small, asymptomatic adenomas.

Medical therapy:

Prolactinomas respond well to dopamine agonists like cabergoline, bromocriptine.

Somatostatin analogs (octreotide) for GH-producing tumors.

Cortisol synthesis inhibitors forACTH-producing tumors.

Surgery:

Transsphenoidal endoscopic approach is standard.

Indicated for large tumors causing mass effect/optic chiasm compression or hormone overproduction unresponsive to drugs.

Radiation therapy:

Adjuvant treatment for residual or recurrent tumors.

Used when surgery or medical therapy is insufficient.

Overall, pituitary adenomas are common intracranial tumors often treated by a combination of surgery, medication, and sometimes radiation, depending on size, hormonal activity, and symptoms.

42. Extraand intramedullary tumors of the spinal cord. Clinic, diagnosis, treatment.

Tumor Types

Intramedullary tumors: Arise within spinal cord substance (ependymomas, astrocytomas, gliomas).

Extramedullary tumors: Arise outside the cord but within dura or epidural space.

Subdural: meningiomas, neurinomas (schwannomas).

Epidural: mainly metastases.

Clinical Features

Intramedullary tumors cause progressive spinal cord syndrome: dissociated sensory loss, muscle atrophy, weakness.

Extramedullary tumors lead to radicular pain, focal sensory loss, motor weakness in root distribution.

Compression symptoms progress from partial cord lesions (e.g. Brown-Sequard) to complete paralysis.

Diagnosis

Clinical presentation: radicular and spinal cord signs.

MRI is the gold standard for localization and characterization.

CSF studies and myelography may also assist.

Bone erosion and foramen enlargement suggest tumor involvement.

Treatment

Surgery

Primary treatment aiming for tumor excision with spinal cord decompression.

Radical resection possible in extramedullary tumors (meningiomas, neurinomas).

Intramedullary tumor resection often limited due to infiltration.

Preoperative planning minimizes neurological damage.

Radiation Therapy

Postoperative or primary treatment when surgery not feasible.

Targets residual or inoperable tumors.

Stereotactic radiosurgery used for select tumors. Chemotherapy

Used primarily in malignant, aggressive, or metastatic tumors.

Effectiveness varies with tumor type. Symptomatic Management

Corticosteroids to reduce edema and relieve pressure.

Pain management, physical rehabilitation.

43.Classification of traumatic brain injury. Light, medium and heavy traumatic brain injury. Treatment.

Classification ofTraumatic Brain Injury

1.By anatomical type:

Open TBI

Non-penetrating (skull fracture without dura tear)

Penetrating (dura mater tear, foreign body, bone fragments inside brain)

Closed TBI

Concussion (shake)

Brain contusion (bruise):

Mild

Moderate

Severe

Compression of brain (hematoma, depressed fracture, foreign body, crush injury)

Diffuse axonal injury (DAI) – damage to white matter fibers, disconnection of cortex from subcortex → always severe

2.By severity (Glasgow Coma Scale = GCS):

Mild TBI (GCS 13–15)

Conscious or mild stunning

Includes concussion and mild brain contusion

Moderate TBI (GCS 8–12)

Deep stunning or stupor

Moderate brain contusion

Early: hematomas, brain edema, raised ICP, seizures, CSF leakage

Late: epilepsy, hydrocephalus, cognitive/motor/speech disabilities, brain atrophy

Treatment Principles

1.Emergency/General

Ensure airway, breathing, circulation (ABC)

Stabilize cervical spine

Oxygen therapy / mechanical ventilation if required

IV access, fluid resuscitation (avoid hypo/hypertension)

2.For Mild TBI

Hospital observation

Rest, analgesics

Control of ICP(head elevation, fluid balance)

3.For Moderate TBI

Hospitalization in neurosurgical ward

Osmotic diuretics (mannitol, hypertonic saline) for edema

Anticonvulsants (for seizures)

Antibiotics (if open TBI)

Surgery if hematoma or depressed fracture

4.For SevereTBI

Intensive care unit (ICU)

Maintain airway + mechanical ventilation

ICPmonitoring; osmotic diuretics, sedation, possible barbiturate coma

Hematoma evacuation / decompressive craniectomy if indicated

Support vital functions (hemodynamics, temp, electrolytes, nutrition)

Summary tip (for exam answer):

Mild: concussion, GCS 13–15, transient symptoms.

Moderate: contusion, GCS 8–12, focal persistent deficits, vitals preserved.