Best Neurosurgical Center

Certain words create interest in almost everyone. Rocket science and Neurosurgery are common words used in most of the deliberations. When it becomes a talk about the best in Neurosurgery it will definitely be an interesting thing to know.
Search for the best Neurosurgical center on Google reveals names of various large hopitals and institutions offering neurosurgical services. The ranking may also be seen on Medscape,  Health US News Report of Best ranked US neurosurgical centers (health.usnews.com › Hospitals › Best Hospitals), etc.
All leading neurosurgical centers across the world provide services in different subspecialties of neurosurgery like Functional Neurosurgery, Cerebrovascular Neurosurgery, Pediatric Neurosurgery, Neurotrauma, Skull Base neurosurgery, Neuro oncology, Spinal Neurosurgery, etc with Neurosurgeons practising different subspecialties. All these subspecialties work as independent units and their work is primarily devoted to a particular branch. Basic & advanced Research and Laboratory task is also done by a dedicated neurosurgical team. Availability of the latest neurosurgical equipments along with world renowned neurosurgeons makes these centers unique.
These centers have achieved present status through decades of hard work & sacrifice. Employing best minds and striving hard to welcome excellent trainees and faculty adds glamour of academic & clinical excellence. Ultramodern infrastructure helps to achieve good clinical outcome of neurourgery.
 

Mayo Clinic, Rochester, Minnesota
                           Bed Count: 1132, Doctors in this specialty: 261

New York–Presbyterian University Hospital of Columbia and Cornell, New York City
                           Bed Count: 2262, Doctors in this specialty: 285

Johns Hopkins Hospital, Baltimore, Maryland
           

                                      Bed Count: 951,  Doctors in this specialty: 162

Massachusetts General Hospital, Boston
                            Bed Count: 779,  Doctors in this specialty: 191

University of California–San Francisco Medical Center
                          Bed Count: 650, Doctors in this specialty: 234


Cleveland Clinic, Ohio
                          Bed Count: 1268, Doctors in this specialty: 192


University of California–Los Angeles Medical Center
          Bed Count: 466, Doctors in this specialty: 223

New York University Langone Medical Center, New York City
                        Bed Count: 791, Doctors in this specialty: 118

Hospitals of the University of Pennsylvania–Penn Presbyterian

Northwestern Memorial Hospital, Chicago
                         Bed Count: 885, Doctors in this specialty: 150

National Hospital for Neurology and Neurosurgery (NHNN), Queen Square, London 

                   UK's largest dedicated neurological and neurosurgical hospital

Leading health care systems provide integrated multispecialty health care with world-renowned health professionals and facilities. The care is not ego-centric but patient-centric. The patient care is highly individualized. A treatment plan is developed for each patient to ensure best neurosurgical result. These institutes are setting the standard of excellence in medical education, research and clinical care. 

Multispecialty clinical care in large hospital setting, excellent infrastructure facilities in operation theaters, dedicated world- renowned neurosurgeons and other health professional, extraordinary laboratory facilities for the research and clinical trials, opportunities of excellent neurosurgical training for the resident doctors and fellows all over the world  have defined these centers of excellence. 

World's best neurosurgical centers are recognized due to clinical accolades, recognition in healthcare groups, contribution to the teaching, training and research and excellent working atmosphere for the faculty and  trainees across the globe.

Although there are many hospitals in other countries which may boast to be the best. But, they lack international vision, do not invite international talents, not open to competition, suffer from inbreeding and employ students from their own college, conventional, lack adequate quality faculty members with interest in subspecialties, and try to be famous just because these centers are relatively larger and better equipped than the adjoining hospitals in that region or country. Laboratory and research facilities are minimal and whenever present usually monopolistic. Majority of Resident doctors, fellows and faculty are from that particular country. A few international fellows may have attended just for the grant or other purpose. The residency training is to used to get manpower and not to produce leaders. Lack of mentorship cripples many neurosurgical training centers across the globe. At many centers teachers compete with students and do not teach the advanced neurosurgical techniques to their students fearing potential competition in future. The attitude of the training center is to restrict the entry of international faculty and residents rather than inviting the best and promising students, residents, fellows and faculty, irrespective of race, religion and citizenship.

If someone wants to explore more,  websites of these hospitals may be viewed.
Don't compete with peers, compete with diseases which cripple the humanity. We are doctors and for us challenges are to find cure of dreaded diseases. Help your peers who work in resource constraints situations and work in anomity but focus on helping patients.  

Excellence is not by chance but it is achieved through hard work, visionary approach and eagerness to consistent progress by best professional who sacrifice their personal interests.

I saw a nice quote on Twitter post of Mr Edward  Relf:

                  “Perfection is not attainable, but if we chase perfection we can catch excellence” 

Thorough Neurological Examination- All in One Page

Never ever presume a neurological diagnosis without interacting with a patient and just by seeing the radiology report or just by listening the patient's complaints. Examine a patient without any presumption & bias, You will always feel rewarded.
Listen to the patient. Patient is the best guide and will provide you the important clue for the diagnosis. History taking is an opportunity to interact with people from diversified background. 
While taking history of a patient who is suspected to have a neurological disorder it should always be prudent to take history pertaining to lesions of brain, spinal cord and peripheral nerves. In this manner you can complete and cover the entire central and peripheral nervous system.
So, if you suspect a lesion of the cerebral hemisheres, History of Seizure, Headache, Vision and , Deterioration of conscious level or loss of consciousness, Weakness of the face or limbs should be taken into detail. 
If you suspect a lesion of cerebellum, then history of imbalance, ataxia and difficulty in walking should always be taken.
And if you suspect a lesion of the brain stem ( Midbrain , pons, medulla Oblongata), the symptoms of multiple cranial nerve deficits ( speech abnormality, nystagmus, difficulty in deglutition, loss of Gag reflex),  and long tract signs ( weakness in limbs, hyperrelexia, increased tone in limbs, positive Babinski sign) are expected.
In patients with lesions of the spinal cord history must include details about  weakness of the limbs, bladder and bowel involvement.

History of headache must include Onset ( sudden, gradual), Site ( holocranial, hemicranial , temoral)Frequency, duration, severity, Character ( Aching, throbbing), timing ( e.g., morning , evening), Precipitating factors (coughing, strenuous work) , Relieving factors ( analgesics, rest) , Associated features ( nausea, vomiting, visual disturbance).
History of Visual Disorder should include onset, frequency, impairment ( uniocular or both eyes, partial or total), diplopia, Precipitaing factor, Associated features
History of Loss of Consciousness may be due to syncope because of cardiac causes or vasovagal shock or due to neurological causes like a part of seizure or neurotrauma or a space occupying lesion in the brain. Loss of consciousness may also be due to low blood sugar level in a patient on diabetic treatment or alcohol or drug abuse.
Speech disorder may be a difficulty in Articulation or Expression or Understanding.
Weakness in the limbs may be Quadriparesis, Hemiparesis or Monoparesis with or without involvement of facial muscles.
History of Sensory system abnormalities  may expressed by the patient as Numbness, feeling of crawling of ants or insects, Tingling or inability to feel a part of the body.
History of cranial nerve deficits may be expressed by the patient as inability to smell, inability to read, loss of vision, diplopia, frequent changes of spectacle, partial closure of the eyelid ( Ptosis)loss of sensation over the face, drooling of saliva from the side, difficulty in closing eye, slurring of speech or change in voice, difficulty in hearing or Deafness, Tinnitus, Vertigo or Dizziness, inability to swallow, inability to shrug and turn face and inability to protrude tongue.

Neurological examination is straight forward, It is like substraction and addition of numbers, like 2+2=4. So, if there is right hemiparesis of body and face and the deep tendon reflexes are increaded, there must be some lesion on the left side of the brain. There is nothing wrong in rechecking the neurological examination findings. But, be sure of your neurological examination findings. Your examination may have a great impact on clinical outcome and plan of the treatment. In Neuroscience most of the things are evident. As students we used to think that many things may be theortical. But, with the advent of newer and advanced neuroradiology, microneurosurgery and functional neurosurgery, lot of procedures are now based on physiological and neuroanatomical localization.
One should begin with systemic examination. See Pallor ( anemia), Icterus ( jaundice), Lymhadenopathy. Anemia may explain many symptoms. Lymhadenopathy may indicate infection, lymphoma or metastasis.

Examine Pulse:  Bradycardia is an omnious sign of raised intrcranial pressure ( ICP)
                           Irregular Pulse may indicate syncope
Blood pressure :  Hypertension may indiacte raise ICP
Respiratory Rate: Irregular Respiration, Bradycardia and Hypertension are parts of Cushing reflex which is due to raised ICP.
Neck rigidity may indicate meningitis or subarachnoid hemorrhage. Restriction of neck movement may be due to cervical spondylosis. One should be very careful while examining a patient with head injury. if a patient is unconscious and his GCS is 8 or less, it is presumed that there may be associated cervical spine injury. So, in severely head injured patient , neck should be immobilized by putting a cervical collar while shifting the patient
Neurological examination begins with higher mental function. orientation to time, place and person should be asked.
cranial nerve examination: Soap may be used to examine olfaction. Vision should be seen in both eyes. If patient is unable to count fingers, then perception of light should be examined with a torch. Pupillary light reflex,ie, constrction of both the pupils when light is projected in eye , gives a clue about both second and third cranial nerves. because second cranial nerve (Optic Nerve) is afferent and third cranial nerve ( Occulomotor nerve) is efferent of this light reflex. Although this is very simple examination but it has great value. We often presume that vision is normal and miss it. A child with craniopharyngima, an adult  with  clinodal meningima or pituitary adenoma may not have any vision in one eye but even patiets or their parents may not be aware about the uniocular visual loss. So, if a doctor misses this finding, there may be catastrophic consequences. As immediately following the surgery , there is natural tendency in everyone to check the vision and it could be concluded that this visual loss be due to surgery. Optic nerve tumor, optic nerve injury, retinal detachmentmay also present with uniocular visual loss.
3,4,6 cranial nerves function may be examined by seeing the conjugate eye movements of both eyes together.
5th cranial nerve, 7th cranial nerve is by examining the face. sensation over the face is mainly by the Vth cranial nerve ( Trigeminal nerve). There are three sensory divisions of Trigeminal nerve ( V1, V2, V3). 7th cranial nerve is the motor supply to the face.
Hearing is through 8th cranial nerve. Ideally 8th cranial nerves should be examined by Tuning forks. If patient hears the rubbing of fingers of the examiner close to each ear, it may give some clue to the intact hearing.
If the gag reflex is intact, 9th and 10th cranial nerves are intact. 
Patient is asked to Shrug the shoulder and turn the face against the resistance to examine sternocleidomastoid and trapezius muscle which are suppled by the spinal accessory nerve.
Protrusion of tongue is possible with the 12th cranial nerve. If Hypoglossal nerve is damaged the tongue deviates to the injured side on protruding. 
Sensory nervous examination should be done before motor examination. Because patients usually are cooperative and sensory system examination is subjective and needs patient,s cooperation.
Motor examination : Movement of all four limbs. Power in all four limbs should be checked separately and should be compared with your own strength. Deep tendon reflexes and tone should also be examined.
Gait; If a patient is able to walk, gait should alsio be examined to complete the thorough neurological examination 

Neuron, Development of Brain

A single neuron is the basic functional unit of the nervous system. It is like a brick in a house. As house is made up of many bricks similarly brain is made of a billion neurons. As cement is needed to provide strength , similarly the neurons are strengthened by neuroglia cells.

A single neuron has has s body (which is also known as soma) with nucleus. Inside  the body there are Nissl granules. From the body arise many projections which carry impulses to the body of the neuron, these tiny projections are called Dendrites ( look like branches of a tree). From the3 body or soma of the neuron a long Axon emerges. The junction of the body and axon is called Axon hillock. Signal and material from the body travel through the axon. Most of the axons are myelinated , i.e., axons are usually covered by a sheath of myelin. In the peripheral nervous sytem myelin is formed by Schwann cells and in the brain it is formed by Oligodendrocytes ( glia cells). This myelin provides white colour and the area of the brain where large number of myelinated fibres are present is called white matter. There are gaps in the myelin sheath along the entire length of axon, these gaps are known as Nodes of Renveer, which allows fast movement of electrical impulses ( action potentials) along the axon. At distal end axon synapses with other neuron or muscle fibre.

This image is a simple depiction to show the development of the brain. 

The brain arises from a tube which is known as neural tube in an embryo. 

In the early embryonic stage of development there are three layers , endoderm, mesoderm and ectoderm. 

Ectoderm is the outer layer of the embryo. Some of the ectoderm cells which are present in the center become destined to form  neural ectoderm. These cells invaginate and convert into a tube which is now, known as Neural tube which is open at both the ends, also known as anterior and posterioral neuropore.

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After 3rd week of embryo development cranial opening of the neural tube which is also known as anterior neuropore , closes. Any abnormality of the closure of the this end may lead to congenital birth anomaly of the brain like anencephaly.

The posterior or caudal neuropore closes at the end of 4th week of embryonic development. Abnormality of the closure of posterior neuropore may lead to spina bifida, split cord malformation. This fact is very significant because when a female becomes aware that she is pregnant most of the neural tube is already developed . A flic acid or folate deficiency has been known to cause neural tube defects, that is why, folate supplementation is advocated in females who plan a pregnancy.

To repeat it again,  brain arises from a tube which is known as neural tube in an embryo. A tube is shown in the diagram mentioned above.

Then the anterior or cranial end of this tube is expanded into three parts which form the brain and caudal or elongated part forms the spinal cord. The three segments of the cranial part of the neural tube are destined to form three major part of the brain. Forebrain, midbrain and hindbrain.

Three cranial expansions are : Prosencephalon ( Forebrain), Mesencehalon (Midbrain) and Rhombencephalon ( Hindbrain). Remember nemonic for 3 sementation stage: PMR. Cavities inside these structures form the ventricles.

Later there are further subdivisions and it becomes of five segments.

Prosencephalon divides into two ;  Telencephalon and Diencephalon. Telencephalon later transforms into two cerebral hemispheres and its cavities become lateral ventricles. Diencephalon may be simply imagined to be like a box , the cavity iside becomes Third ventricle. he lateral walls of this box become 2 thalami, floor becomes hypothalamus, roof becomes epithalamus and part becomes subthalamus.

Mesencephalon changes into midbrain.

Rhombenecphalon subdivides into two subdivision; Metencephalon and Myelencephalon. From Metencephalon Pons and Cerebellum develop. Myelencephalon transforms into medulla oblongata. The distal part of the neural tube gives rise to spinal cord.

HEADACHE

Pain in head is called headache. Almost everybody experiences headache. One episode of mild headache may be due to exertion, stress or some causes which may not be alarming and you can afford to neglect.
Headache is a very common symptom. Almost everyone experiences headache at some stage of life. Despite of being so common it becomes sometimes it becomes a matter of concern.
So, one should not panic and should analyze the severity of the problem and proceed further for seeking the medical attention & investigations.
Lot of literature is available on the causes of headache but I would like to overly simplify this topic so that one can have an overview.


If headache is associated with exertion at the end of the working day and is over the vertex, frontal or occipital region of the skull and is relieved on taking rest or head massage, one should not worry.
if someone is very stressed and there is obvious stress then there can be psychogenic headache. That person should adopt the less stressful lifestyle and practice relaxation exercise , yoga  , and very rarely psychotherapy or some medicines may be required.


Maxillary or frontal sinusitis also causes headache.
Redness of eyes, frequent sneezing, cold , allergy may also cause headache.Cluster headache occurs in clusters.


In older persons headache may occur due to hypertension and temporal arteritis.



Refractive errors like myopia and hypermetropia may also cause periorbital pain and headache especially in young children going to school. So vision examination should also be done in patients complaining of headache.
If a child complains of headache it may due to refraction error in vision. Common cause is myopia when someone complains of difficulty in seeing distant things. child may not read the letters written on blackboard in a class and there may be decrease in scholastic performance in school. Another refractive error is hypermetropia which is difficulty in reading the small letters. Although, this is a common problem in people over 40 years of age, it is becoming more common in childrenm because of too much indulgence in mobile games, computer games and less outdoor play activities.
So common cause of Persistent headache is refractive error of vision.

Other common cause is sinusitis. Such patients will have frequent history of nasal infections, pain over the bony air sinuses in skull. Maxillary sinusitis, frontal air sinusitis may be diagnosed by tenderness and X-Ray Skull. Sometimes CT scan may be needed. Most of the patients are treated by antibiotics.

Common cause of headache is tension headache. In this type is headache pain is over the vertex, i.e, top of the head. Since the muscles are under continuous tension , such headache will diminish if head massage is given.

Hypertension, anemia may also cause headache.

Migraine is very common and typically paroxysm of throbbing type of headache on irregular intervals, unilateral, associated with vomiting. Migraine is more common in females. There are many variants of migraine.Migraine is the diagnosis of exclusion. Before labelling a ptient with this diagnosis all other causes must be ruled out, like anemia, brain tumor, hemorrhage, infection. CT scan or MRI of the brain rules out any intracranial mass occupying lesion.  It is normally hemicranial,i.e., involes one half of the head. It is usually throbbing headache and associated with nauses and vomiting. Migraine is recurrent and gradually the duration between episodes become less.


What should not be missed?
Any physician or person should not ignore headache due to brain tumor and subarachnoid hemorrhage due intracranial aneurysm rupture.
How to recognize headache due to brain tumor? Usually progressive, associated with vomiting, temporarily relieved after vomiting, may be associated with blurring of vision ( due to papilloedema), or other neurological deficit.
How to recognize headache due to subarachnoid hemorrhage caused by rupture of intracranial aneurysm? It is sudden onset severe headache ( bolt from blue, thunderclap headache which a patient in the age group of 4th - 5th decade, says that he or she had never experienced such type of headache in life time. Sometimes headache may not be so severe and it is called warning leak. There may be associated neck rigidity.
What is the most valuable investigation in the management of headache??
If  Visual examination of the patient is performed  and  Non contrast CT scan of the head is advised one will never be guilty of missing a life threatening brain condition like SAH ( subarachnoid hemorrhage and brain tumor) and it will guide the further course of treatment.

Sudden onset severe headache in a person of about 40 to 50 years of age which is so intense as patient describes that he or she had never experienced such headache in his or her life time,"Bolt from Blue," is typical of spontaneous subarachnoid hemorrhage ( SAH) due to rupture of intracranial aneurysm.

Head trauma, cervical spondylosis may also cause headache.

Headache associated with seizures is alarming. CT scan or MRI of the brain must be done.

Cranio-Vertebral Junction ( CV Junction)

Cranio-Vertebral Junction is the bony junction of the skull and vertebral column. It is formed by Clivus, Occipital bone and C1 and C2 vertebra.

This area is important as any abnormality in this area may lead to compression over the cervico- medullary junction, which is the junction of the cervical region of the spinal cord qnd medulla oblongata.

The abnormality at this region could be congeital anomaly or acquired.

This is simple diagram of the sagittal view shows location of CV Junction. TOO is abbreviation for transoral odontoidectomy . This surgery is done through oral cavity . Anterior arch of Atlas vertebra ( first cervical vertebra)  lies just anterior to the odontoid process of Axis vertebra ( 2nd cervical vertebra). Any dislocation of Atlanto-Axial Joint ( Atlanto axial dislocation -AAD) may compress over the medulla Oblongata, which lies just posterior to the Dens of the C2 vertebra.

Stability of the CV junction is mainly due to ligaments. 

The anterior atlanto-occipital membrane is the cranial extension of the anterior longitudinal ligament. It extends from anterior margin of foramen magnum to anterior arch of C1.

Posterior Atlanto-occipital membrane connects posterior margin of the foramen magnum to the posterior arch of Atlas.

Tectorial Membrane is the upward continuation of posterior longitudinal ligament. It connects the dorsal surface of the Dens of the Odontoid process of C2 vertebra anterior lip of the Foramen magnum.

Apical odontoid Ligament connects the tip of Dens to the anterior lip of Foramen Magnum.

Alar Ligament  connects side of the Dens to occipital condyles.

Transverse Ligament is the horizontal component of the Cruciate ligament which traps or straps or binds the Dens anteriorly against the C1. It is the strongest ligament.

Cerebral Angiography, Digital Substraction Angiography ( DSA)

Invention of Cerebral Angiography is an important historical landmark in evolution of Neuroradiology and Neurosurgery. 

In 1927, Dr Egas Moniz developed a technique of injecting a contrast material into the arteries . The dye or contrast used was Thorotrast. 

When a contrast or dye which is soluble in blood is injected into the common carotid artery the blood vessels become visible and look opaque on background of X-ray image of skull.  This technique of imaging the blood vessels of the brain is known as cerebral angiography. Rapid sequences of the X-ray images are obtained after injecting contrast into common carotid artery. Similar images could also be obtained when contrast is injected into the femoral artery.  Cerebral angiography allows visualization of blood vessels in and around the brain.

Before 1927, may be called  X-ray era, i.e., in the begining of 20th century, neurosurgery was possible by localization of the lesion by neurological examination and using the X-ray techniques. Application of X-rays in investigations like ventriculogram, encephalography, myelogram were used to localize lesions. 
Roentgen invented application of x-rays imaging in 1896.
Walter Dandy described pneumoencephalography and pneumoventriculography in 1918.
In 1921, myelography was introduced when jean Sicard a French clinician and his pupil Jacques Forestier injected analgesics into the spine of a patient suffering from low back pain and subsequently found that the oil they used as a carrier for the analgesic, lipiodol, was radio-opaque.
The invention of myelography encouraged the Portuguese neurologist Egas Moniz to develop ' Arterial Encephalography'.

After 1927, the dignostic ability of the physician changed dramatically. Using the technique of cerebral angiography, Norman Dott, in 1931,  demostrated cerebral aneurysm on cerebral angiography and later, Walter Dandy was able to operate a case of intracranial aneurysm, in 1933.

Cerebral angiography depicts the vessels along with X-ray of the skull. 

Later, with the use of computer, the background of skull image could be substracted. So, the artery or vein is visualized better. So, the technique of substracting the bony details  is called Digital Substraction  Angiography  ( DSA ). But, if somebody wants to see relation of the aneurysm against the bony landmark of the skull, it is still possible in DSA because the bone image was substracted digitally and computer again can depict the same.  Thus, DSA is gold standard investigation for detection and surgical planning for intracranial aneurysms.

                                                     Image of DSA , here the internal carotid artery is seen , the image is lateral view of the skull but the bony details have been digitally substracted so that one can focus on the ICA and its branches. ICA is seen as in neck, carotid siphon as a loop and intracranial branches. The first intracranial branch of ICA   which runs anteriorly is ophthalmic artery. Second intracranial branch which runs poseriorly is Posterior communicating artery. Anterior Choroidal artery is another intrcranial branch of ICA which is seen to traverse posteriorly on lateral view of DSA.

First investigation for investigating a suspected case of spontaneous subarachnoid hemorrhage is CT scan of the brain. Non-contrast CT scan reveals the site of the bleed, like blood in the anterior inter-hemispheiric space is suggestive of SAH due to rupture of anterior communicating artery. Then, the second investiation is to know the detail of the aneurysm, which is done by DSA.

Since, DSA is an invasive procedure, so the another option is to go for CT angioprphy. MR angiography ( MRA) is a noninvasive procedure and it does not require any injection. But MRA is less sensitive than CT angiography and DSA.

Digital Substraction Angiography ( DSA) involves passing a catheter in the femoral artery over the anterior aspect of the thigh in the femoral triangle and then advancing the catheter upward. Then, injection of a contrast material ( Dye) through a catheter. Once catheter is at the arch of aorta it needs to be negotiated to the carotid artery and vertebral artery. So, anatomy of arch of aorta is important.

                                         The contrast is injected into the Femoral artery on right side and then catheter is advanced upward into the arota under the fluroscopic guidance. At the arch of aorta the catheter is negotiated into the artery depending upon the need of DSA. On the right side there is first branch of arch of aorta, brachiocephalic trunk. Right common carotid artery is a branch of brachiocephalic trunk.
Left common carotid artery is a direct branch of arch of aorta. Left subclavian artery is also a direct branch of arch of aorta and vertebral artery is a second branh of subclavian artery.

Spontaneous subarachnoid hemorrhage due to ruture of intracranial aneurysm commonly occurs in the age group of 40-60 years with a peak incidence in the fifties.
Aneurysm bleed is the commonest cause of spontaneous SAH ( about 85%). 
Other common causes of spontaneous SAH are:  artriovenous malformations ( AVM), hemorrhage from tumor, pituitary apoplexy, vasculopathy ( like collagen vascular disease, amyloid angiopathy , arterial dissection) , haematological ( anticoagulant therapy, leukaemia, hepatic or renal disease induced coagulopathy ) and drugs like cocaine, amphetamine and ephedrine.

Subarachnoid hemorrhage (SAH) is a neurological emergency  characterized by hemorrhage into the subarachnoid space, and may present as sudden, severe headache ( as bolt from blue ) which patient may state that he or she may have never experienced before. Sentinel hemorrhage occurs in about 40% of patients with SAH. This is also known as " warning leak". Nuchal rigidity or meningismus is noted in 50% of patients due to meningeal irritation following SAH. Hemiparesis, focal neurological deficits including cranial nerve deficits are other common features. Fundus examination may reveal papilloedema and subhyaloid hemorrhage.

On the basis of GCS and Focal deficit, the severity of the clinical presentation of the patients may be graded into 5 grades , according to the World Federation of Neurological Surgeons  (WFNS).
In WFNS Grade 1 the patients are of GCS 15/15 and have no focal deficit. And, if patient's GCS is 13 or 14 then it is Grade 2. And patient has a focal deficit with a GCS of 13 or 14, his grade becomes Grade 3.   poor GCS of 7-12 makes a patient of grade 4 and if patients GCS is 6 or less then his garde becomes 5, irrespective of the presence or absence of focal deficit.

NCCT ( NECT) , i.e., Noncontrast or nonenhanced CT scan of the barin is the first investigation of choice. It shows hyperdensity in the subarachnoid space and may indicate the site of bleed. or example, anterior communicationg artery aneurysm bleed shows blood or hyperdensity in the anterior interhemispheric cisterm. the ruture of the Middle cerebral artery may present with hematoma in the temporal lobe or in the sylvian fissure of that side.

Fischer's grading of SAH on the basis of CT findings:
In Grade 1: there is no detectable blood on CT scan
Grade 2 : Diffuse thin  SAH  less than 1 mm thickness, & if thickness of clot is more than 1mm then it is labeled as Grade 3.
Grade 4: Intraventricular or intracerebral clot with diffuse or no subarachnoid hemorrhage

If  CT scan is normal and still there is strong suspicion of SAH, then the next  investigation is Lumbar Puncture, which reveals xanthochromia. 

Common locations of intracranial aneurysms include Anterior communicating artery ( 30%), the junction of the ICA and Pcom ( 25% ), MCA bifurcation ( 20% ), ICA bifurcation ( 7.5%). Around 7% arise from the basilar bifurcation and 3% arise from the PICA, a branch of vertebral artery.

Digital Substraction Angiography ( DSA) or CT Angiography ( CTA) is the investigation of choice. MR angiography ( MRA) does not use any contrast and it is a good non invasive screening investigation.

Source: Wikipedia

Understanding of CNS Tuberculosis- Three Landmark Papers

It is amazing and inspiring to see the excellent contributions of founders of medicine. While working on CNS tuberculosis I found that our present understanding of the tuberculosis is based on the works of physicians who existed about a century ago. Their contributions are immense and very encouraging to us.  The following three landmark papers helped in the understanding of aetiology , pathogenesis and treatment of tuberculosis of the central nervous system.

1. Green PH. Tubercular meningitis. Lancet 1836; II: 232–35.

2. Koch R. Die aetiologie der tuberculosis.
Berlin Klinische Wochenschrift 1882; 19: 221–30.

3. Rich AR, McCordock HA. The pathogenesis of tuberculous
meningitis. Bull John Hopkins Hosp 1933; 52: 5–37.

Before the demonstration of a tuberculous bacteria by Robert Koch, Green PH had published a paper in Lancet in 1836, describing a new diagnosis called tubercular meningitis.

May 14, 1836

Volume 26
Number 663
p225-256

Originally published as Volume 2, Issue 663

Green PH. Tubercular meningitis. Lancet 1836; II: 232–35.

In this paper Green P.H., President of the Society of Foreign Physicians, Paris, France, coined the new term in medicine " Tubercular Meningitis. In this paper there is description of clinical presentation of tubercular meningitis and acute hydrocephalus and post mortem findings of the patients showing caseation and exudates.


Koch R. Die aetiologie der tuberculosis. Berlin Klinische Wochenschrift 1882; 19: 221–30.

Robert Koch (1843-1910) was a German master of medicine. He got Nobel Prize in Medicine. he is regarded as Founder of science of Bacteriology. In 1876, he demonstrated Anthrax bacillus and in 1882 he demontrated tubercle bacillus.

          Robert Koch: German physician & Pioneering Microbiologist ( demonstated bacteria causing Anthrax, Cholera ans tuberculosis)




Rich AR, McCordock HA. The pathogenesis of tuberculous meningitis. Bull John Hopkins Hosp 1933; 52: 5–37.

Arnold Rice Rich (1893-1968) was born in Birmingham, Alabama in USA on March 28, 1893. He studied at University of Virginia and John Hopkins. He worked as Professor of pathology at John Hopkins , Baltimore, USA. He was excellent teacher and researcher. His contribution in medical sciences is immense. His contributions include the understanding of pathology of jaundice, pathogenesis of tuberculosis.

                                                                       A R Rich
                                Source http://www.medicalarchives.jhmi.edu/images/rich.jpg

This paper by AR Rich is the outcome of clinical and animal experiments. this paper described the occurrence exudates in tuberculosis.



Sources:

http://www.nasonline.org/publications/biographical-memoirs/memoir-pdfs/rich-arnold.pdf

Robert Koch: centenary of the discovery of the tubercle bacillus, 1882
ALEX SAKULA, From Redhill General Hospital, Surrey
Thorax 1982;37:246-251

Wikipedia: Robert Koch

http://www.medicalarchives.jhmi.edu/images/rich.jpg

http://www.medicalarchives.jhmi.edu/papers/rich.html

Vladimir Bekhterev and Ludwig Puusepp

Vladimir Mikhailovich Bekhterev (1857-1927)

The first operating room at the neurology department of the Russian Military Medical Academy was established in 1897 by the famous Russian neurologist and psychiatrist Vladimir Bekhterev. According to Bekhterev, neurology should become a surgical speciality like gynaecology or opthalmology and neurologists will take a knife in their hands [1]. He was an outstanding Russian neurologist, psychiatrist, psychologist, morphologist, physiologist authored over 1000 scientific publications. He created a new multidimensional multidisciplinary scientific branch - psychoneurology. He also proposed "biopsychosocial" model in the interpretation of human diseases [2].

Both Ivan Pavlov and Bekhterev independently developed a theory of conditioned reflexes which describe automatic responses to the environment. What was called association reflex by Bekhterev is called the conditioned reflex by Pavlov, although the two theories are essentially the same [3].

Vladimir Bekhterev (source: wikipedia)

Bekhterev's pupil Ludwig Puusepp (1875-1942) became the first full-time Russian neurosurgeon ("surgical neurologist"). He headed the first university course in surgical neurology in the world organised in 1909 at Bekhterev's Psychoneurological Institutte in St. Petersburg and became professor of surgical neurology in 1910. The role of neurologist might be illustrated by the development of a sterotactic instrument named "encephalometer" designed by D. Zernov in 1889 and improved by G. Rossolimo in 1907 [1].

Ludwig Puusepp: world's first professor of Neurosurgery ( Source ; Wikipedia)

Sources: 

1.Lichterman BL. Roots and routes of Russian neurosurgery (from surgical neurology towards neurological surgery).J Hist Neurosci. 1998 Aug;7(2):125-35.

2.Akimenko MA.Vladimir Mikhailovich Bekhterev. J Hist Neurosci. 2007 Jan-Jun;16(1-2):100-9

3. Wikipedia

Cerebellopontine angle and Retromastoid Craniectomy

Retromastoid craniectomy is an important neurosurgical approach for operating lesions of the cerebellopontine angle ( CP angle).

Commonest CP angle tumor is acoustic schwannoma  Other common tumors of CP angle are CP angle meningioma and epidermoid. 

Retrosigmoid region is the part of the cranium situated just behind the sigmoid sinus and below the transverse sinus.

The lateral cerebellomedullary and cerebellopontine cisterns are encountered in this approach.

Three important arteries are encountered bilaterally in this region: 

Posterior inferior cerbellar artery (PICA),

Anterior inferior cerbellar artery (AICA), &

Superior cerebellar artery (SCA)

PICA arises from the vertebral artery and is seen in relation to the lower cranial nerves. Occasionally, it may reach high enough to come in contact with the lower limit of the VII/VIII complex.

AICA arises from the basilar artery and distal part is seen in relation to the VII/VIII complex. This nerve-related segment is divided into premeatal, meatal, and postmeatal parts. The meatal part forms a loop ( meatal loop) which travels along the VII/VIII complex for a variable distance toward the internal acoustic meatus. Several nerve-related branches of AICA exist: the internal auditory artery, recurrent perforating arteries, subarcuate artery , and cerebellosubarcuate artery. The internal auditory artery is the most constant branch of the AICA.

The SCA arises from the basilar artery quadrification courses back along the side of the mid brain and pons , and is seen in the cerebellopontine angle in front of the Vth cranial nerve.

The veins of the posterior fossa can be divided into superficial , deep , and bridging veins. Anterior hemispheric veins , veins of the cerebellopontine fissureand middle cerebellar peduncular veins, lateral medullary and lateral mesencephalic veins, and petrosal bridging veins.

Petrosal veins are divided into superior and inferior veins which drain into superior or inferior petrosal sinus.

The superior petrosal veins are the most prominent bridging veins of the posterior fossa. They drain blood from a large part of the cerebellar hemisphere and brainstem. Superior petrosal veins are divided into a lateral, intermediate or medial group based on their relation to the site of drainage into the superior petrosal sinus and IAM.

Cranial nerves V through XII are seen in this approach. CN V is a stout nerve arising from the upper and outer aspect of the anterior pons. Its motor component arises as a separate rootlet just anterior to the main nerve , and both quickly merge to form a single nerve. Loops of the SCA can be seen in front of the nerve at this level.The nerve courses anteriorly and outward to cross the petrous apex and enter into the Meckel,s cave.

Cranial nerve VI arise medially at the pontomedullary sulcus. It courses up the surface of the clivus exiting the posterior fossa through Dorello’s canal. It enters the posterior cavernous sinus on its way through the middle cranial fossa to the orbit.

The VII/VIII complex, with the nervus intermedius in between, arises from the pontomedullary junction surrounded by the same fascial sheath. They course backward, downward, and outward toward the internal acoustic meatus.

Cranial nerves IX, X, XI arise as a linear series of rootlets from just below the pontomedullary junction in the anterolateral medullary sulcus. After their origin, they converge outward and backward toward the jugular foramen. CN XII lies in close proximity to the vertebral artery-PICA junction. Its many rootlets exit though the hypoglossal canal.

Retromastoid craniectomy can be performed with the patient in sitting, park-bench, three-quarter prone position, lateral or supine position.
The description by Robert L. Martuza for surgery of acoustic neuroma in supine position is straight forward. The patient is positioned supine with one or two folded soft cotton blankets beneath the ipsilateral shoulder and padding beneath the knees and is secured with one or two belts to allow the table to be rolled if necessary during surgery. Too much turning of the body can place the shoulder in a position that interferes with surgery.
The head should be fixed in Mayfield or Sugita frame.
A retroauricular lazy 'S' or linear or C shaped incision is made in the scalp which is paramedian and about 5 mm medial to the mastoid notch.
Dr Robert L. Martuza suggests a linear incision approximately 3 cm behind the insertion of the pinna and going from approximately 1 cm above the tip of the pinna to 1 cm below the ear lobe. The muscles are then divided inferiorly and self retaining retractors are placed.
The sigmoid sinus lies beneath the mastoid groove.
The transverse sinus and sigmoid sinus generally curve around the asterion. Therefore, a burr hole is placed medial to the asterion.
Craniectomy is done after placing a burr hole.  After craniectomy the inferior edge of the transverse sinus and the medial edge of the sigmoid sinus should be defined with the help of rongeurs. The transverse sinus lies above the upper limit of craniectomy and sigmoid sinus is lateral to the craniectomy.typically a K-shaped incision or linear incision about 2 cm medial to the edge of the sigmoid sinus  is made in the dura with the edges being based on the sinus.
After retracting the cerebellar hemisphere medially and superiorly cisterna magna comes into the view. The arachnoid of this cistern is opened and CSF is drained and this maneuver relaxes the cerebellum, obviating the need for further retraction.

Middle neurovascular complex in CP angle includes AICA, pons and middle cerebellar peduncle. The AICA arises at the pontine level and courses in relationship to the abducens, facial & vestibulocochlear nerve to reach the surface of the middle cerebellar peduncle, where it courses along the cerebellopontine fissure and terminates by supplying the petrosal surface of the cerebellum. Common operations in this region are for removal of acoustic schwannomas and for the relief of hemifacial spasm.

Acoustic schwannomas, as they expand, may involve a majority of the cranial nerves, cerebellar arteries, and parts of the brain stem.

Lateral view of skull to show Asterion: Meeting point of Parietomastoid suture, Occipitomastoid suture and lambdoid suture.   

Sources:

1. Chapter: Suboccipital retrosigmoid surgical approach for vestibular schwannoma ( acoustic neuroma) by Robert L. Martuza in Schmidek & Sweet operative neurosurgical techniques- indications, methods & results. Alfredo Quinones- Hinojosa. 6^th ed. (Elsevier Saunders) 

2. Rhoton Cranial anatomy and surgical approaches, Neurosurgery, Albert L. Rhoton, Jr  

3. Oerative Neurosurgical Anatomy by Damirez T. Fosset and Anthony J. Caputy ( Thieme publication)
4, Wikipedia

Neurosurgical Management of CNS Tumors: Review of Recent Advances

Due to technological advancements and better understanding of brain tumors, there had been a significant improvement in the clinical outcome of brain tumors. The majority of the brain tumors are now diagnosed at a very early stage. CT scan or MRI of the brain is a very common diagnostic tool and help to diagnose any lesion inside the brain.
All the brain tumors need not be operated. Non invasive single dose radiation therapy like Gamma knife or Cyberknife is a noninvasive way of treating small lesions of the brain.
Stereotactic biopsy helps in minimal invasive way of diagnosing brain tumor.
Stereotactic Radiotherapy ( SRT) is used to treat malignant lesions of the brain. Even multiple metastasis of systemic cancers of the body to the brain can be treated with surgery and SRT.
Meningioma which constitute about 15% of all the primary brain tumors can be excised completely without any recurrence.
So, if somebody is diagnosed as a case of brain tumor, he or she should not lose hope. Unlike other tumors of the body, the brain tumors are not labeled as cancer and non cancer. Rather, there are differerent grades of the tumor ( WHO Grade 1 to IV). Grade 1 tumors are usually benign and do not require chemotherapy or radiotherapy.
Neuro-oncology constitutes the major part of clinical practice of neurosurgeons. Almost every neurosurgeon operates and manages cases of CNS tumours. Many advances have occurred in last few decades and now many options are available for investigating and treating such lesions. Translational research has provided hope for the better clinical outcome in future. MRI with contrast , MR spectroscopy, PET scan are the new investigative modalities to detect neoplasis and metastasis . Immunotherapy, vaccine therapy, molecular based targeted therapy, Bevacizumab, Temozolomide, Brachytherapy, stereotactic radiotherapy, stereotactic biopsy of the lesion, gamma knife are the new treatment options for treating CNS tumors.

Classification of CNS tumors by WHO (World Health Organization) in 2007 identifies 7 broad categories of CNS tumors:
1. tumors of neuroepithelial tissue
2.tumors of cranial and paraspinal nerves
3. tumors of the meninges
4. lymphomas & hematopoietic neoplasms
5.germ cell tumors
6. tumors of the sellar region
7. metastatic tumors

This framework is necessary to have an idea about all CNS tumors.

It is very important to use authentic terms for the cns tumors and have an overall view about all the tumors of the central nervous system. Various nomenclatures and classifications are used for description. Therefore, it is imperative to know what is most authentic and easiest way to remember. 

The pathological classification of cns tumors is the most common and most practical way of nomenclature and classification of such tumors.

CNS tumors, especially gliomas, contrary to the other cancers of the body , cannot be classified like Benign or Malignant or  Cancer and Non cancer or like Benign lesion of the Breast ( Fibroadenoma) and Cancer of the breast ( Ca Breast) , or Benign Prostrate Hyperplasia (BPH) and Cancer of the Prostrate. 
On the contrary, the Gliomas or Astrocytomas are classified on the basis of features of neoplasia- like cellular atypia, nuclear proliferation, vascular proliferation & necrosis. So, there is a grading of neoplasia. 
Cushing and Bailey classification was an earlier effort to classify brain tumors. 
World Health Organization ( WHO) classification of  tumors of central nervous system ( 2007)  is a comprehensive, and  authentic  source of reference.

1. Tumours of neuroepithelial tissue

1.1. Astrocytic tumours

        

        Pilocytic astrocytoma  & Subependymal giant cell astrocytoma (WHO grade I)

       

        Pilomyxoid astrocytoma & Pleomorphic xanthoastrocytoma (WHO grade II)

        

         Diffuse astrocytoma (WHO grade II) 

                        Variants:  protoplasmic,   gemistocytic,   fibrillary,  mixed

       

         Anaplastic astrocytoma (WHO grade III)

        

         Glioblastoma (WHO grade IV)

                                         a. Giant cell glioblastoma

                                         b. Gliosarcoma

    

          Gliomatosis cerebri (WHO grade III)

1.2. Oligodendroglial tumours

                 Oligodendroglioma (WHO grade II)

                 Anaplastic oligodendroglioma (WHO grade III)

1.3. Oligoastrocytic tumours

                 Oligoastrocytoma (WHO grade II)

                 Anaplastic oligoastrocytoma (WHO grade III)

1.4. Ependymal tumours

                 Subependymoma &  Myxopapillary ependymoma (WHO grade I)

                 Ependymoma (WHO grade II)

                 Anaplastic ependymoma (WHO grade III)

1.5. Choroid plexus tumours

                     Choroid plexus papilloma (WHO grade I)

                     Atypical choroid plexus papilloma ( WHO grade II)

                     Choroid plexus carcinoma (WHO grade III)

1.6. Other neuroepithelial tumours

                   Astroblastoma (WHO grade I)

                  Chordoid glioma of the third ventricle (WHO grade II)

                  Angiocentric glioma (WHO grade I)

1.7. Neuronal and mixed neuronal-glial tumours

                    Dysplastic gangliocytoma of cerebellum (Lhermitte-Duclos),

                    Desmoplastic infantile astrocytoma/ganglioglioma,

                    Dysembryoplastic neuroepithelial tumour, 

                    Gangliocytoma ,

                    Ganglioglioma

                    Papillary glioneuronal tumour

                    Rosette-forming glioneuronal tumour of the fourth ventricle, & 

                    Paraganglioma are WHO grade I tumors.

                    Central neurocytoma & Extraventricular neurocytoma , Cerebellar liponeurocytoma   (WHO grade II)

                    Anaplastic ganglioglioma (WHO grade III)

                                 

1.8. Tumours of the pineal region

               Pineocytoma (WHO grade I)

               Pineal parenchymal tumour of intermediate differentiation (WHO grade II, III)

               Pineoblastoma (WHO grade IV)

               Papillary tumors of the pineal region (WHO grade II, III)

1.9. Embryonal tumours

              Medulloblastoma (WHO grade IV)

              Medulloblastoma with extensive nodularity (WHO grade IV)

              Anaplastic medulloblastoma (WHO grade IV)

              CNS Primitive neuroectodermal tumour (WHO grade IV)

              CNS Neuroblastoma (WHO grade IV)

              Atypical teratoid/rhabdoid tumour (WHO grade IV)

2. Tumours of cranial and paraspinal nerves

              Schwannoma (WHO grade I)

              Neurofibroma (WHO grade I)

              Perineurioma (WHO grade I, II, III)

              Malignant peripheral nerve sheath tumour (MPNST) (WHO grade II, III, IV)

3. Tumours of the meninges

3.1 Tumours of meningothelial cells

 Meningioma

                   Variants ( Subtypes ): meningothelial,  fibrous (fibroblastic),  transitional (mixed),  psammomatous,  angiomatous,  microcystic,  secretory,  clear cell,  chordoid,  lymphoplasmacyte-rich, and  metaplastic

 Atypical meningioma (WHO grade II)

 Anaplastic meningioma (WHO grade III)

3.2 Mesenchymal tumours

 Lipoma , Angiolipoma ,Liposarcoma,  Leiomyoma,  Leiomyosarcoma, Solitary fibrous tumour ,  Fibrosarcoma , Rhabdomyoma, Rhabdomyosarcoma,Chondroma , Chondrosarcoma,  Osteoma,Osteosarcoma, Osteochondroma, Angiosarcoma, Kaposi Sarcoma, Ewing Sarcoma - PNET 

 Malignant fibrous histiocytoma

 Hibernoma

 Haemangioma 

 Epithelioid hemangioendothelioma

 Haemangiopericytoma & Anaplastic haemangiopericytoma (WHO grade III)

3.3 Primary melanocytic lesions

                      Diffuse melanocytosis

                      Melanocytoma 

                      Malignant melanoma 

                      Meningeal melanomatosis 

3.4 Other neoplasms related to the meninges

                     Haemangioblastoma (WHO grade I)

4. Tumors of the haematopoietic system

                       Malignant Lymphomas

                        Plasmocytoma

                        Granulocytic sarcoma

5. Germ cell tumours

                             Germinoma

                             Embryonal carcinoma

                             Yolk sac tumour

                             Choriocarcinoma

                             Teratoma

                             Mixed germ cell tumours

6. Tumours of the sellar region

                                Craniopharyngioma (WHO grade I)

                                Granular cell tumour (WHO grade I)

                                Pituicytoma (WHO grade I)

                                Spindle cell oncocytoma of the adenohypophysis (WHO grade I)

7. Metastatic Tumours


I have made an effort to create an outline and curtail the details so that any doctor can have an overview of all the tumors of CNS. The details of all such tumors should  be read in conjunction with the radiological findings which is more interesting and easy.
The most recent classification of CNS is proposed by WHO in 2016.

WHO (2016) Classification of Tumors of Central Nervous System

In year 2016, for the first time, the World Health Organization ( WHO) classification of CNS tumors uses molecular parameters in addition to histology to define many tumor entities. Major restructuring has been done in diffuse gliomas, medulloblastomas and other embryonal tumors. It has added newly recognized neoplasms, and has deleted some entities, variants and patterns that are no longer have diagnostic and/or biological relevance.

Summary of changes in new classification

• Major restructuring of diffuse gliomas, Medulloblastomas, other embryonal tumors & incorporation of genetically defined entities
• The term “primitive neuroectodermal tumor” is removed
• Incorporation of a genetically defined ependymoma variant - RELA fusion positive
• 
  
  Addition of
            Newly recognized entities, variants and patterns have been added:
                            1.  IDH-wildtype and IDH-mutant glioblastoma 
                            2. Diffuse midline glioma, H3 K27M–mutant
                            3. Embryonal tumour with multilayered rosettes, C19MC-altered
                            4. Ependymoma, RELA fusion–positive
                            5. Diffuse leptomeningeal glioneuronal tumor
                            6. Anaplastic PXA
                            7. Epithelioid glioblastoma  
                             8. Glioblastoma with primitive neuronal component
                             9. Multinodular and vacuolated pattern of ganglion cell tumor
  Deletion of
              Gliomatosis cerebri
              Protoplasmic and fibrillary astrocytoma variants
              cellular ependymoma variant
              Primitive Neuroectodermal tumor
  
  

• Addition of Brain invasion as a criterion for atypical meningioma
• Restructuring of solitary fibrous tumor and hemangiopericytoma ( SFT/HPC) as one entity
• Expansion & clarification of entities included in of Nerve sheath tumors, with addition of hybrid nerve sheath tumors & separation of melanotic schwannoma from other schwanomas
• Expansion of entities included in hematopoietic/lymphoid tumors of the CNS ( lymphomas & histiocytic tumors)
                       
                                     NEW CLASSIFICATION
  Diffuse astrocyic and oligodendroglial tumors

• Diffuse astrocytoma, IDH-mutant
                          Gemistocytic astrocytoma, IDH-mutant

•  Diffuse astrocytoma, IDH-wildtype
•  Diffuse astrocytoma, NOS
• Anaplastic astrocytoma, IDH-mutant
• Anaplasticastrocytoma, IDH-wildtype
• Anaplastic astrocytoma, NOS

• Glioblastoma, IDH-wildtype
                       Giant cell glioblastoma
                       Gliosarcoma
                       Epitheloid glioblastoma

• Glioblastoma, IDH-mutant
• Glioblastoma, NOS

• Diffuse midline glioma, H3 K27M-mutant
• Oligodendroglioma, IDH-mutant and 1p/19q-codeleted
• Oligodendroglioma, NOS
  
  

• Anaplastic Oligodendroglioma, IDH-mutant and 1p/19q-codeleted
• Anaplastic oligodendroglioma, NOS
  
  

• Oligoastrocytoma, NOS
• Anaplastic Oligoastrocytoma, NOS
  Other astrocytic tumor

• Pilocytic astrocytoma
                   Pilomyxoid astrocytoma

• Subependymal giant cell astrocytoma
• Pleomorphic xanthoastrocytoma
• Anaplastic pleomorphic xanthastrocytoma
  Ependymal tumors

• Subependymoma
• Myxopapillary ependymoma
• Ependymoma
                  Papillary ependymoma
                  Clear cell ependymoma
                  Tanycytic ependymoma

• Ependymoma, RELA fusion-positive
  Anaplastic ependymoma
  Other gliomas

• Choroid glioma of the third ventricle
• Angiocentric glioma
• Astroblastoma
  Choroid plexus tumors

• Choroid plexus papilloma
• Atypical choroid plexus papilloma
• Choroid plexus carcinoma
  Neuronal & mixed Neuronal-glial tumors

• Dysembryoplastic neuroepithelial tumor
• Gangliocytoma
• Ganglioglioma
• Anaplastic ganglioglioma
• Dysplastic cerebellar gangliocytoma ( Lhermitte-Duclos disease)
• Desmoplastic infantile astrocytoma and ganglioglioma
• Papillary glioneuronal tumor
• Rosette forming glioneuronal tumor
• Diffuse leptomeningeal glioneuronal tumor
• Central neurocytoma
• Extraventricular neurocytoma
• Cerebellar liponeurocytoma
• Paraganglioma
  Tumor of the Pineal region

• Pineocytoma
• Pineal parenchymal tumor of intermediate differentiation
• Pineoblastoma
• Papillary tumor of pineal region
  Embryonal tumors
  Medulloblastoma, genetically defined
                         Medulloblastoma, WNT activated
                         Medulloblastoma, SHH-activated and T53-mutant
                         Medulloblastoma, SHH-activated and T53-wildtype
                         Medulloblastoma,  non-WNT/non SHH
                                  Medulloblastoma,  group 3
                                  Medulloblastoma, group 4
  Medulloblastoma, histologically defined
                         Medulloblastoma, classic
                         Medulloblastoma, desmoplastic/nodular
                         Medulloblastoma with extensive nodularity
                         Medulloblastoma, large cell/anaplastic
  Medulloblastoma NOS

• Embryonal tumor with multilayered rosettes, C19MC-altered
• Embryonal tumor with multilayered rosettes, NOS
• Medulloepithelioma
• CNS Neuroblastoma
• CNS ganglioneuroblastoma
• CNS embryonal tumor, NOS
• Atypical teratoid/ rhabdoid tumor
• CNS embryonal tumor with rhabdoid features
  
  
  Tumors of cranial and paraspinal nerves
  Schwannoma
            Cellular Schwannoma
            Plexiform Schwannoma
            Melanotic Schwannoma
  Neurfibroma
            Atypical neurofibroma
            Plexiform neurofibroma
  Perineurioma
  Hybrid nerve sheath tumors
  Malignat peripheral nerve sheath tumor
              Epitheloid MPNST
              MPNST with perineurial differentiation
  
  
  Meningioma

• Meningioma
• Meningothelial meningioma
• Fibrous meningioma
• Transitional meningioma
• Psammomatous meningioma
• Angiomatous meningioma
• Microcystic meningioma
• Secretory meningioma
• Lymphoplasmacyte-rich meningioma
• Metaplastic meningioma
• Chordoid meningioma
• Clear cell meningioma
• Atypical meningioma
• Papillary meningioma
• Rhabdoid meningioma
• Anaplastic ( malignant) meningioma 
  
  
  Mesenchymal, Non-meningothelial tumors

• Solitary fibrous tumor/hemangiopericytoma
• Hemangioblastoma
• Hemangioma
• Epitheloid hemangioendothelioma
• Angiosarcoma,
• Kaposi Sarcoma,
• Ewing sarcoma/ PNET
• Lipoma
• Angiolipoma
• Hibernoma
• Liposarcoma
• Desmoid type fibromatosis
• Myofibriblastoma

•  Inflammatory myofibroblastic tumor
• Benign fibrous histiocytoma
• Leiomyoma
• Leiomyosarcoma
• Rhabdomyoma
• Rhabdomyosarcoma
• Chondroma’
• Chondrosarcoma
• Osteoma
• Osteochondroam
• Osteosarcoma
  Melanocytic tumors

• Meningeal melaonocytosis
• Meningeal melanocytoma
• Meningeal melanoma
• Meningeal melanomatosis
  Lymphoma

• Diffuse large B-cell lymphoma of the CNS 
• Immunodeficiency-associated CNS lymphoma
                            AIDS-related diffuse large B-cell lymphoma
                            EBV-positive diffuse large B-cell lymphoma, NOS
                            Lymphomatoid granulomatosis 

• Intravascular large B-cell lymphoma 
• Low-grade B-cell lymphoma of the CNS 
• T-cell & NK/T cell-lymphoma of the CNS 
• Anaplastic large cell lymphoma , ALK-positive 
• Anaplastic large cell lymphoma , ALK-negative 
• MALT lymphoma of the dura
  Histiocytic tumors

• Langerhans cell histocytosis
• Erdheim-Chester disease
• Rosai-Dorfman disease
• Juvenile xanthogranuloma
• Histiocytic sarcoma
  Germ cell tumors

• Germinoma
• Embryonal carcinoma
• Yolk sac tumor
• Choriocarcinoma
• Teratoma
                   Mature, Immature

• Teratoma with malignant transformation
• Mixed germ cell tumor
  Tumors of the sellar region
  Craniopharyngioma
               Admantinomatous craniopharyngioma
               Papillary craniopharyngioma
  Granular cell tumor of sellar region
  Pituicytoma
  Spindle cell oncocytoma
  Metastatic tumors

Neurosurgery is the cornerstone of the management of tumors of the brain and spinal cord. Because glioma annd metastasis constitute majority of tumors, very judicious approach is required for the diagnosis and treatment of such lesion. Many options are available but they may be costly, unnecessary and harmful. A very small low grade glioma be an incidental finding and surgery may not be required. A small neoplastic lesion of less than 3 cm may be treated with gamma knife which is a non surgical treatment and utilizes precise and focussed single dose radiation over a deep seated lesion in the eloquent area of the brain.

About 4 decades ago, whole brain radiotherapy and steroids were the main treatment modality for treating brain metastasis. But now few brain metastatic lesions may be excised safely and stereotactic radiotherapy can be given postoperatively, reducing the morbidity in a patient.

Advances in the skull base approaches have made the neurosurgery relatively safer, and few tumors can be excised completely. This may be true in cases of intracranial meningiomas.