Neurosurgery Brain Tumors - Meningioma

• 1. tumors of neuroepithelial tissue
• - astrocytoma (Glioma),
• - oligodendroglioma,
• - oligoastrocytoma,
• - ependymoma,
• - choroid plexus papilloma,
• - medulloblastoma,
• - CNS neuroblastoma

• 2. tumors of cranial and paraspinal nerves
• - Schwannoma
• - Neurofibroma
• - Perineuroma
• 3. tumors of the meninges 
• - Meningioma 

• 4. lymphomas and hematopoietic neoplasms
• - Malignant lymphoma
• - Plasmacytoma

• 5. germ cell tumors
• - Embryonal carcinoma
• - Yolk sac tumor 
• - Choreocarcinoma
• - Teratoma 

• 6. tumors of the sellar region
• - Craniopharyngioma 
• - Pituitary carcinoma 
• - Pituitary adenoma

• 7. metastatic tumors
• - Lung cancer, specially small cell 
• - Breast carcinoma 
• - Melanoma 
• - RCC

• Gliomas are the most commonly occurring  primary brain tumor.
• Glioblastoma multiforme (GBM) is the most malignant form of glioma causing 3–4% of all cancer-related deaths. 
• GBM is grade IV astrocytoma. 
• Glioblastomas are generally found in the cerebral hemispheres of the brain, but can be found anywhere in the brain or spinal cord.
• This tumor represents about 15.4% of all primary brain tumors and about 60-75% of all astrocytomas.
• They increase in frequency with age, and affect more men than women.
• Only three percent of childhood brain tumors are glioblastomas.

• Primary or de novo:
• - More common in older patients (mean age 55 yrs)
• - Short clinical history (<3 months)
• - More aggressive than secondary glioblastomas
• - More common 

• Secondary:
• - Secondary glioblastomas are those which arise from pre-existing lower grade gliomas
• - Younger age group (mean age 40 years)
• - Slower clinical course
• - Very aggressive

• 1. Slowly progressive neurologic deficit, usually motor weakness
• 2. Headache
• 3. Generalized symptoms of increased intracranial pressure, including headaches, nausea and vomiting, and cognitive impairment
• 4. Seizures

Neurologic symptoms and signs can be either general or focal and reflect the location of the tumor

• o CT head
• - irregular thick margins
• - irregular hypodense centre representing necrosis
• - marked mass effect
• - surrounding vasogenic oedema
• - haemorrhage occasionally seen

• o Magnetic resonance imaging, with and without contrast (study of choice)
• - T1 phase shows hypo to isointense mass within white matter central heterogeneous signal (necrosis, intratumoural haemorrhage)
• - T2/FLAIR shows hyperintense, surrounded by vasogenic oedema, flow voids occasionally seen

• o MR spectroscopy - typical spectroscopic characteristics include
• - choline: increased
• - lactate: increased
• - lipids: increased
• - N-Acetyl Aspartate: decreased [@ NAA Li Cho La]

o Positron emission tomography

Cytoreductive surgery followed by external beam radiation (40 Gy whole-brain + 15-20 Gy to the tumor bed delivering a total of - 60 Gy to the tumor) has become the standard against which other treatments are compared. 

Patients older than 70 years: Less aggressive therapy is sometimes considered, using radiation or temozolomide alone

• Slow growing, extra-axial tumor, usually benign, arise from arachnoid (not dura).
• Most commonly located along falx, convexity, or sphenoid bone.

• Meningiomas are the most common primary intracranial tumors, and most remain asymptomatic throughout the patient's life.
• Most often present with headache and mental status changes
• Jacksonian seizure and progressive monoplegia
• Visual symptoms, focal seizures, or mental status changes

• MRI - Occasionally may be isointense with brain on T1WI and T2WI, but most enhance with gadolinium. Brain edema may or may not be present. Calcifications appear as signal voids on MRI. "Dural tail" is a common finding.
• CT - Homogeneous, densely enhancing mass with broad base of attachment along dural border.
• Angiography - Classic pattern: "comes early, stays late" (appears early in arterial phase, blush persists beyond venous phase). Meningiomas characteristically have carotid artery feeders.

 

Most (but not all) are cured if completely removed, which is not always possible. Surgery is the treatment of choice for symptomatic meningiomas. Incidental meningiomas with no brain edema or those presenting only with seizures that are easily controlled medically may be managed expectantly with serial imaging as meningiomas tend to grow slowly, and some may "burn out" and cease growing. 

• General principles of meningioma surgery:
• 1. early interruption of the blood supply to the tumor
• 2. internal decompression (using ultrasonic aspirator, cautery loops . . . )
• 3. dissection of the tumor capsule from the brain by cutting and coagulating vascular and arachnoid attachments while infolding the tumor into the area of decompression with minimal retraction on adjacent brain
• 4. removal of attached bone and dura when possible

• Radiation therapy (XRT) - Generally regarded as ineffective as primary modality of treatment. Some surgeons reserve XRT for malignant (invasive),
• vascular, rapidly recurring ("aggressive"), or non-resectable meningiomas.

Grade // Degree of removal

I // macroscopically complete removal with excision of dural attachment and abnormal bone (including sinus resection when involved)

II // macroscopically complete with endothermy coagulation (Bovie, or laser) of dural attachment

III //  macroscopically complete without resection or coagulation of dural attachment or of its extradural extensions (e.g. hyperostotic bone)

IV // partial removal leaving tumor in situ

v // simple decompression (± biopsy}

• o Spina bifida occulta
• o Spina bifida cystica - Meningocele and Meningomyelocele
• o Encephalocele
• o Anencephaly
• o Dermal sinus
• o Tethered cord
• o Syringomyelia
• o Diastematomyelia
• o Lipoma involving the conus medullaris

Meningomyelocele is a neural tube defect, presenting as a protrusion of the spinal cord and meninges, due to incomplete closure of the neural tube.

It represents one of the most common birth defects.

Meningomyelocele is often associated with type II Arnold-Chiari malformation.

At birth, it presents as a midline defect in the posterior aspect of the skin and vertebrae, associated with an outward protrusion of the cord, meninges and other neural components.

Meningomyelocele is commonly associated with Chiari type II malformation, which may result in symptoms of compression of the brainstem and cervical spinal cord including apnea, dysphagia, nystagmus, laryngeal and pharyngeal paralysis, stridor, and upper limb paresthesias. This malformation may also cause cerebellar compression and dysfunction resulting in ataxia

Children with meningomyelocele often present with joint contractures, spinal and lower limb deformities. These may be attributed to intrauterine malpositioning, muscle imbalance, poor posture, progressive neurologic deficits, and reduced joint function. Children with meningomyelocele are also commonly of short stature, attributable to skeletal abnormalities including spinal cord and vertebral abnormalities, lower extremity contracture, and endocrine involvement

Genetic and several acquired abnormalities

1. Chromosomal abnormalities including trisomy 13, 18, and 21

2. Maternal diabetes, maternal age, socioeconomic class, season of conception, maternal alcohol toxicity, maternal use of anticonvulsants, intrauterine hyperthermia, geographic location, maternal folate and zinc deficiencies.

3. Conceptions which occur in spring time are more likely to be associated with anencephaly and spina bifida in the fetus

Neural tube defects occur as a result of an interruption in the neurulation process.

• The process of neural formation occurs in two stages;
• -  primary stage - neural plates elevate and close in towards each other, forming a neural tube
• - secondary stage - further neural development, including the formation of the terminal fibres of the spinal cord. This stage is described as the stage of canalization.

Defects or interruptions in the primary stage of neurulation cause the open neural tube defects, while defects in the secondary neurulation are responsible for closed neural tube defects.

1. assessment and management of lesion:

• A. measure size of defect
• B. assess whether lesion is ruptured or unruptured
• - ruptured: start antibiotics (e.g. nafcillin and gentamicin; discontinue 6 hrs after MM closure, or continue if shunt anticipated in next 5 or 6 days)
• - unruptured: no antibiotics necessary
• C. cover lesion with telfa, then sponges soaked in lactated ringers or normal saline (form a sterile gauze ring around the lesion if it is cystic and protruding) to prevent desiccation
• D. Trendelenburg position, patient on stomach (keeps pressure off lesion)

• 2. Surgical consideration -
• - MM defect closure and VP shunting is the surgery of choice. 
• - Early closure of MM defect is not associated with improvement of neurologic function, but evidence supports lower infection rate with early closure. MM should be closed within 24 hrs whether or not membrane is intact.
• - Orthopedic surgical procedures may be necessary for debilitating musculoskeletal abnormalities presenting in this condition. Such procedures aim at improving the quality of life of the patient.

Approximately 70% of meningomyelocele cases can be prevented by increasing serum folate levels just before conception and up to the seventh week of gestation, at which time, the neural tube has closed completely

• CT scan - 50 centiGray (cGy) 
• X-ray - 0.5 cGy

• Tab Nimodipine 60mg 6 times a day 
• Inj NS @ 120-150 ml/hr 
• Inj Phenytoin 100ml in 100ml NS TDS 
• Tab Codeine Phosphate 30mg QID 
• Syp Laxil 20ml BD

10-20 microgram/ml

Ankle foot orthosis boot

• <3 mmol/liter- normal/acute viral meningitis  
• 3 to 6 mmol/liter - partially treated bacterial meningitis (PTBM),
• >6 mmol/liter - Acute bacterial meningitis