Skull Base Neurosurgery in one page : Easy facts to develop insight

Every neurosurgical trainee should develop an insight about the nuances of skull base neurosurgery. If you are able to make a bur hole in skull, you have already taken first step in understanding and practicing skull base neurosurgery.
Aim of skull base neurosurgery is to reach deeper regions of the brain with minimal retraction of the brain tissue. Prolong retraction of brain parenchyma leads to edema, ischemia and brain damage and, in turn,  increases post operative morbidity.

One should learn to draw the lateral view of skull depicting zygoma, pterion and orbit.

Fronto-temporal craniotomy or pterional craniotomy is very useful for approaching middle cranial fossa lesions. But this often requires prolong temporal lobe retraction, so adding orbito-zygomatic craniotomy makes the job easy. Therefore, little more work on skull base helps to reduce morbidity.

To understand the skull base surgery, one should know that cranial cavity can be divided into anterior, middle and posterior cranial fossa ( learn to draw a line diagram showing ACF, MCF & PCF).

ACF floor can further be zoomed to see midline structures like crista galli, olfactory groove, planum sphenoidale and tuberculum sellae. Laterally roof of the orbit forms the floor of anterior cranial foosa (ACF). The anterior skull base tumors can be meningiomas (olfactory groove meningioma, planum sphenoidale meningioma or tuberculum sellae meningioma. For CSF rhinorrhea repair, excision & repair of intranasal encephalocele, exciosion of intracranial extension of ethenioneuroblastoma and excision of intracranial fungal granulomas extending into nasal cavity, and chordoma of the floor of the ACF, one should know bicoronal scalp inciosion,  bifrontal craniotomy just above the orbit and anterior to the coronal suture, exteriorization of frontal air sinus, clipping and cutting of the superior sagittal sinus close to crista galli and opening the dura and retracting base of the frontal lobe backwards.

Mid sagittal image of the MRI is very easy to understand the relation of intracranial structures to the nasal cavity and how Trans nasal transphenoidal and transoral odondoidectomy  is done. This image will also help you understand the supracerebellar infra tentorial approach for operating pineal tumor

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Like usefulness of fronto temporal craniotomy for anteriorly placed lesions, midline sub occipital craniotomy is basic and of equal importance for operating lesions of midline posterior fossa structures. Scalp incision is made from external occipital protuberance to the C2 spinous process. Scalp is retracted and a bur hole is made in the occipital squama and the suboccipital craniectomy is done. Dura is opened in 'Y' shaped manner to avoid injury to the occipital sinus. Midline suoccipital craniectomy is done for operating Medulloblastoma, Cerebellar ependymoma, 4th ventricular tumor, posterior fossa decompression for Chiari malformation.If lesion is situated laterally like cerebellar astrocytoma the paramedian suboccipital craniectomy is done. far lateral, retromastoid cranectomy are done for other posterior fossa lesions.

TNTS is abbreviation for for transnasal transsphenoidal surgery & 

TOO stands for transoral surgery

In Frontotemporal craniotomy, at the supraorbita ridge care should be taken to identify and preserve the supraorbital nerve and vessel passing through the supraorbital foramen or notch. These can be released with the aid of a chisel or drill. A bur hole is made at the McCarty keyhole. The sphenoid ridge is made as flat as possible down to the level of the meningo-orbital artery.

In orbital osteotomy , the peroorbita is separated from the roof of the orbit for a distance of 3 cm posteriorly from the supraorbital ridge, and it is also separated along the lateral wall of the orbit. A sagittal cut is made in the roof of the orbit from the cranial to the orbit side to a depth of at 3 cm posterior to the supraorbital ridge. A second cut is made above the zygomatic process of the frontal boneand extended posteriorly as deep as possible within the orbit. Third cut is a coronal cut made across the roof of the orbit to connect the previous cuts. In orbitozygomatic osteotomy, this coronal cut across the roof of the orbit extends laterally  from the sagittal cut to the inferior orbital fissure. A third cut is made parallel to, but several millimeters above, the zygomaticomaxillary suture.

In Transbasal approach,  after making the McCarty keyhole bilaterally, a bifrontal craniotomy is done as close to the floor of the frontal fossa as possible. The posterior wall of the frontal air sinus is removed and thereby cranializing the sinus.The medial floor of the frontal fossa, including the roof of the ethmoidal air cells, is removed . The lateral margins of the the bone removal are the medial walls of the orbit. In Extended Transbasal approaches,  a bone cut is made through the nasofrontal suture, sagittal cuts are made just medial to the supraorbital notch on each side. This allows en bloc removal of the central portion of the supraorbital bar.

Trans-sphenoidal approach is used for sellar lesions , especially pituitary adenoma, through nasal cavity.

In Anterolateral Extradural/ Intraduralapproach for cavernous sinus, after cranio-orbitozygomatic osteotomy, the optic canal is unroofed and its medial wall drilled. The superior orbital fissure should be u roofed and the anterior clinod process resected. The floor of the middle fossa between the SOF and the foramen rotundum is drilled and the foramen is enlarged. The middle meningeal artery is identified and followed to the foramen spinosum. It is coagulated and divided , thus allowing the dura to be elevated from the floor of the middle fossa. The dura is dissected in a lateral to medial fashion until the greater superficial petrosal nerve (GSPN) is encounterd.To avoid the risk of injury to the facial nerve, the GSPN is transected and the bone of the Glassock’s triangle is drilled away, exposing the posterior loop of the ICA and freeing it from its bony canal to obtain proximal control. The dura is then ready for opening.

In Preauricular Subtemporal-Infratemporal approach, a temporal craniotomy is performed, temporal dura is stripped from the floor of the middle fossa and arcuate eminence is identified. This is the posterior extent of the dissection. The dural separation is then continued anteriorly to reach the foramen spinosum, where the MMA can be seen as it enters the cranial cavity. Zygomatic osteotomy is done . Anteriorly a V-shaped cut is made at the level of the frontozygomatic and zygomaticomaxillary suture. The posterior cut is made to include the condylar fossa. This cut is also V-shaped, with the apex of V just short of the foramen spinosum and the limbs spanning the anterior and posterior extent of the zygomatic root. V3 (mandibular) and  V2 ( maxillary) divisions of the fifth nerve then are exposed at the foramen ovale and rotundum, respectively. The GSPN may be cut close to the facial hiatus.

Transpetrosal approach include translabyrinthine and transcochlear approaches require division of the external ear canal and mastoidectomy.

Retrosigmoid craniotomy or craniectomy is used for surgery of.cerebellopontine angle tumors. A retroauricular skin incision is made.

Midline or Paramedian suboccipital craniectomy is used for approaching posterior foassa lesion.

Extreme lateral approach is used for vertebral and vertebral- basilar junction aneurysm.

For approaching the posterior third ventricular lesions and Pineal tumors, supracerebellar infratentorial, occipital transtentrorial approach and interhemispheric approaches are useful.

Sources: Operative Neurosurgical anatomy by Damirez T. Fossett &Anthony J.Caputy (Thieme)





Advancements in Management of Dementia

Dementia is a progressive impairment of cognitive function that eventually becomes severe enough to interfere with social behaviour and with the patient’s work. It affects memory, language expression, learning, spatial constructive abilities behaviour and thinking to varying degrees. Some 1% of persons aged 60-64, but 30% of those over 85, suffer from dementia. The age- specific  prevalence of dementia roughly doubles every 5 years after age 60. Persons with large fund of knowledge and varied interests are less likely to become demented in old age¹.

The psychopathological and neurological deficits include memory impairment (mostly recent memory ), personality change, impairment of abstract thinking and judgement, apraxia, and agnosia.

Diagnosis of dementia is based on a thorough case history, including interview of persons close to the patient,  neuropsychological examination and  Mini-mental status examination (MMSE) ¹.

Causes of dementia include degenerative diseases of the brain ( Alzheimer’s disease is the commonest), Cerebrovascular disease ( Multi- infact dementia), infectious diseases ( AIDS-Dementia complex, Prion diseases like CJD ), Metabolic diseases like Wilson’s disease), Neoplasia  ( such as  as brain tumors), Epilepsy, deficiency states ( Vitamin B12 deficiency), toxic conditions ( heavy metal poisoning), mental illnesses ( severe depression), hydrocephalus, Demyelinating disease ( Multiple Sclerosis). So, the ancillary tests for evaluation of a patient with dementia may include:  CT scan or MRI of the brain, ESR, CRP, CBC, PBS, Na, K, Ca, BUN, Glucose, Serum electrophoresis, Hepatic enzymes, HIV, Syphilis serology, TSH, Vitamin B12, folic acid, EEG, ECG, Lumbar Puncture , SPECT or PET, Antibodies ( like ANA, anti-dsDNA,etc), heavy metals tests, ammonia , cortisol, Lyme, herpes simplex serology, genetic analysis¹.

The social and economic impact of dementia  is enormous  and  its consequences on the caregivers is equally troublesome. Moreover, the treatment of memory and cognition deficts  due to varied pathologies is challenging for the physicians.  But, now we stand on the threshold of a new age in dementia care ².

Prospect of pharmacotherapy and surgical treatment of dementia is bright. The clinical trials on the beneficial effects of drugs  have provided some hope  to the patients with Alzheimer’s disease. Physical training  and cognitive support are also needed to achieve functional improvement. Studies have shown that physical activity stimulates angiogenesis, synaptogenesis and neurogenesis. Physical activity prevents dementia and conversion from mild cognitive impairment ( MCI) to dementia. A balanced diet and healthy foods predominantly vegetables, unsaturated fatty acids , grains and fish  lower risk of dementia. Keeping weight within normal limts should be encouraged. The consumption of high doses of alcohol must be avoided. The use of antihypertensive can reduce the risk of cognitive decline and dementia. Stopping smoking should be recommended at any stage of life.

Although current data is lacking to justify the use of  drugs  in prevention and treatment of various subtypes of dementia.  However, the robust clinical trials and research in this field have offered some hope to the patients suffering from dementia. A reduction in acetylcholine and choline acetyltransferase occurs in dementia type consequently impairing cholinergic pathways. Ginkgo biloba, Nicergoline, Vipocetine, Co-dergocrine mesylate ( Hydergine) and other ergoloid mesylates, Piracetam, Pentoxiphyllne , Citicholine , Cerebrolysin, Cholinesterase inhibitors ( Rivastigmine, Donepezil),  glutamate receptor antagonists ( Memantine) Galantamine, Calcium channel blocker ( Nimodipine, Nicardipine) are few therapeutic agents  which can be believed to be beneficial for preventing and treating dementia on theretical grounds.

Carotid revascularization in patients with symptomatic carotid stenosis reduces risk of stroke recurrence . The carotid revascularization can be done either by surgical approach, carotid endarterectomy  (CEA) or endovascular by carotid artery stenting (CAS). Cognitive domains include memory, executive function and language³.

Deep brain stimulation ( DBS) is a therapeutically effective neurosurgical method  for treating dementia. DBS of the fornix  and nucleus basalis of Meynert  can influence activity in the pathologic neural circuits that underlie  Alzheimer’s disease ( AD) and  Parkinson disease dementia ^4,5.

Some of the causes of dementia are amenable to cure. Virtually any metabolic or endocrine derangement can cause cognitive problems. Neurosyphilis, AIDS,,Whipple disease,, vitamin B12  , folate and thiamine deficiency, and hypothyroidism,.

Neurosurgical patients  with Brain tumor, chronic subdural hematoma and normal pressure hydrocephalus ( NPH) may present with dementia. Normal pressure hydrocephalus produces a clinical triad of  progressive dementia , urinary incontinence and gait disturbance.The dementia is of subcortical type, with marked cognitive slowing, in the absence of focal cortical deficits. Chronic subdural hematoma ( SDH) patients may also present with dementia and bur hole evacuation of hematoma is the treatment of choice. Frontal  lobe tumors like meningioma  can be excised and patient is revieved of the symptoms of memory deficits. Similarly, a CSF diversion procedure in patients of NPH can treat dementia.
In Normal pressure hydrocephalus, MRI of the brain may show features of cerebral atrophy like shrunken brain with prominent sulci and gyri and so there will be enlargement of the ventricles. But, the ventriculomegaly will be disproportionately larger when compared with the extent of cerebral atrophy. Moreover, there will be some transependymal cerebrospinal fluid transudation in the form of periventricular high signal on T2-weighted images and FLAIR images. Consequtive three day CSF tapping by Lumbar puncture with removal of about 30 ml CSF each day leads to improvement in patients of NPH and is a good indication to do a CSF diversion procedure like low pressure ventriculoeritoneal shunt surgery or Lumbperitoneal shnt surgery.

Access to the supportive care for physical , emotional and social needs of dementia patients should be the priority of the health care institutions.  Occupational therapist, Physiotherapist, Speech therapist , Neurosychologists, Medical anthropologist , Psychiatrist, Neurologist and Neurosurgeon are important components of multidisciplinary management, care and neuropsychological rehabilitation of the patient with dementa. These intervention will help the patient and their caregivers for coping with problems associated with dementia.

References:

1.     Neurology ( Thieme flexibook on clinical sciences), By  Mark Mumenthaler, Heinrich Mattle with Ethan Taub, Thieme, 4^th ed. New York. 

2.      Editorial : Azheimer’s disease: a treatment in sight? Jornal of Neurology, Neurosurgery and Psychiatry, Dr  Simon Lovestone, Robert Howard.  1995:59:66-567

3.      Treatment of vascular dementia . Brucki SMD, et al. Dementia Neuropsychol  2011 December; 5(4):275-287

4.      Stimulate or degenerate: Deep brain stimulation of the Nucleus basalis of Meynert in Alzheimer’s dementia. Laxton AW, Lozano AMD.  World Neurosurg, 2012

5.      Neurosurgical treatment of dementia: A review,  Hardenacke K, et al. World Neurosurg, June, 2012.

6.      Dementia : Differentiation and Rehabilitation Strategies By Carole Lewis and Susan Staples.

Neuropsychology

Neuropsychologist may assess and help patients with ADHD, Conduct disorder, oppositional defiant disorder, Eating disorder, Anorexia Nervosa, separation anxiety disorder, generalized anxiety disorder, panic disorder, agoraphobia, OCD, and other neuropsychiatric conditions.  

Clinical neuropsychologists assess and treat the cognitive and emotional needs of patients requiring neurosurgery conditions such as brain injury, brain tumors, hydrocephalus, etc.  Neuropsychologist assesses neurocognitive functioning of neurosurgical patients.

As a neuropsychologist one can critically assess changes in patients’ memory, attention, language, and other functions that help determine the course of treatment and rehabilitation and can contribute in clinical neuroscience research on quality of life issues in patients with neurosurgical disease.

Neuropsychological assessments help patients and physicians in multiple ways, including:

• Pinpointing mild or subtle neurocognitive deficit;
• Predicting the course of a disease and recovery rate;
• Assisting in determinations about a patient’s return to school or work, and;
• Helping patients and their families understand the effects of the disease process, including coping techniques, which may aid in diagnosis.

Source: http://www.pennstatehershey.org/web/neurosurgery/patientcare/specialtyservices/neuropsychological

 

Utilization of standard and flexible batteries in clinical evaluation

Dimensional –categorical approach to neuropsychological evaluation approach to neuropsychological evaluation is contingent on a dimensional as opposed to a modular brain model . The idea that the brain is modular is an old one, dating back at least to Gall who believed that different faculties were represented in different regions of the cortex. The opposing view, that the cortex functions as a unified whole, at least with regard to higher mental functions, has always challenged the modular one.  

Fixed batteries in neuropsychological assessment

Halstead- Reitan Neuropsychological Battery

Recent development in the two most frequently utilized fixed neuropsychological batteries , the Halstead –Reitan and the Luria-Nebraska Neuropsychological batteries : In HRB: Development of new summary scores: General Neuropsychological Deficit scale ( GNDS), the Left neuropsychological Deficit scale ( LNDS), & the Right Neuropsychological Deficit scale ( RNDS).

GNDS is a summary scale based on 42 variables from the HRB that characterizes the degree of overall impairment of neuropsychological functioning . this summary score ranges in classification from normal through mild , moderate , and severe degrees of impairment .

Comprehensive Norms for an Extended HRB ( CNEHRB)

Halstead Russel Neuropsychological Evaluation System ( HRNES)

Wechsler Adult Intelligence Scale

WAIS-R

LURIA-NEBRASKA NEUROPSYCHOLOGICAL BATTERY ( LNNB)

The LNNB-1 has undergone changes since 1980. Addition of delayed memory scale, intermediate memory scale

Tests developed by process oriented neuropsychologists utilize tests include the current 60-item version of the Boston Naming Test, Boston Diagnostic Aphasia Examination, the Cancellation test, Delayed Recognition Span Test & non verbal mood scales.

Existing tests that are administered in a manner reflecting the process approach include the WAIS-R as a neuropsychological instrument , Wechsler Memory scale, Hooper Visual Organization test, Rey-Osterreith Complex Figure, Recurrent Series Writing and Multiple Loops.

Neuropsychological Examination of select populations

Child Neuropsychological assessment; tests within cognitive domains of intelligence, achievement, language, visual –spatial and construction, somatosensory, and motor functions, attention , memory and learning and problem solving. Standardized interviews , broadband rating scales, self report inventories.

 Neuropsychological evaluation of the elderly (with dementia)

Minnesota Multiphasic Personality inventory (MMPI), Millon Clinical Multiaxial Inventory, Conner’s Continuous Performance Test

Computer assessment allows for the assessment of performance efficiency, response time, and variability. Automated assessment in the evaluation process. Lack of education, limitation of evaluating cognitive domains such as language and memory, cost, unfamiliarity.

 

Neuropsychological rehabilitation

Modern day cognitive rehabilitation (CR) spans a number of disciplines , including speech pathology, occupational therapy, special education, physical medicine, neurology , cognitive psychology, cognitive neuroscience, rehabilitation psychology and neuropsychology. Rehabilitation has developed as a result of contributions of all these professions and incorporates many different theories and techniques.

Understanding of brain restoration of function

Theory of Phrenology (Franz Gall) 18^th century: gall’s theory was almost completely incorrect, it was perhaps a springboard for those who would later accurately describe localization of brain function.

In the mid-1800s, Paul Broca, the French physician, anatomist, and anthropologist, began his work. He described an intuitive rehabilitation program to restore lost skills in an adult patient who became unable to read aloud. Building on Broca’s work, the great German neuropsychiatrist Carl wernicke was one of the first to conceptualize brain function as a series of regions that were dependent on interconnected neural pathways. This localization and interconnection concept became a fundamental element of clinical psychology and CR.

As the 20^th century dawned, prominent American neuropsychologist Shepherd Franz was using scientific methodology to study motor learning in hemiparesis and effectiveness of therapy in clients with aphasia, making him pioneer in neuropsychological rehabilitation. Like Broca, Franz noticed that his aphasic patients looked like they were learning new skill rather than relearning an old habit. This observation established a precedent for using techniques that focus on learning new skills to compensate for abilities lost or diminished due to brain damage. During and after the two World Wars, Germany & Austria led the way in developing brain injury rehabilitation centers to treat wounded soldiers and German psychologist Kurt Goldstein, Soviet neuropsychologist Alexander Luria,  British neuropsychologist Oliver Zangwill made significant contributions. In 20^th century Yehuda BenYishay (1970), Muriel Lezak ( 1986), Sohlberg and Mateer made siginificant contribution in the field of CR. Neuropsychological rehabilitation centers in US,  CR, neuropsychological rehabilitation interventions, cognitive-didactic treatment approach, functional-experimental approach, systematic CR program: Reitan Evaluation of Hemispheric abilities and Brain Improvement Training (REHABIT) is patient specific & comprises of 3 levels of information processing : (a) attention, concentration, & memory, (b) lateralized processes ( verbal or visuospatial &, (c) higher order abilities such as abstraction and logical analysis. Sohlberg and Mateer’s ( 1989, 2001) attention process training ( APT) series, Robertson’s  (1996) specific cognitive retraining model for addressing executive dysfunction called as the Goal Management Training method. Carter ( 2000) frontal lobe dysfunction, Metzler-baddley & Jones 2010, Children). Memory, visuospatial , language function. Memory Clinic, Emotional dysregulation. Neuropsychological rehabilitation is  a broader field than CR because it encompasses “ amelioration of emotional, psychosocial, & behavioral deficits caused by an insult to the brain” in addition to CR.

Available literature on PubMed, PsychInfo, MEDLINE: Psychotherapy with CR, meditation therapy, catastrophic thinking (e.g., distortion in which patient imagines the worst possible outcome of an event or situation), hypersensitive to one’ error failure to distinguish between normal ordinary error in functioning and more serious errors, are likely caused by brain injury. Psychodynamic approach, disruption of patient’s sense of self ( “ego” identity) : fractured ego identity

[ Phrenology (Oxford dictionary) : The study of shape of the human head, which some people think is a guide to a person’s character]

Use of technology in CR

Memory notebooks

Cognitive prosthetics: smart phones, ipads, PCs, Computerized attention training, Virtual reality programs, telerehabilitation

Incorporation of neuroimaging with neurocognitive techniques, treatment protocol.

A protocol for assessment, psychotherapy and neurorehabilitation for neurosurgical patients may contribute towards holistic neuropsychiatric care provided by the  interdisciplinary team.

The role of psychotherapy and neurorehabilitation is well established in the treatment of brain injured patients. There is need for better understanding of neuropsychological profile of the patients with other intracranial space occupying lesions like brain tumors. There is paucity of literature about the neuropsychological profile of the patients undergoing cranial neurosurgery for brain lesions. The assessment of neuropsychological profile of neurosurgical patients may help in recognizing the subtle changes due to brain lesions, awareness of patient’s emotional distress, designing compensatory strategies and patient’s coping skills, and evolving psychoeducational techniques for neurosurgical patients.

Neurological findings , radiographic findings, neurosurgical plan and neuropsychological assessment will be part of comprehensive presurgical evaluation of the patient. The neuropsychological evaluation will provide essential quantitative and qualitative data about the patient’s neuropsychological and emotional status.

Neuropsychological domains: Effort/motivation,  attention/ concentration, speed of information, processing, motor functioning, verbal functioning, visuospatial functioning,  memory, concept formation, reasoning, executive functioning, awareness, personality composition and psychological distress, estimate of premorbid intelligence.

Sample Tests: California Verbal Learning Test (CVLT) for Effort/ Motivation

                          WAIS-IV, for other domains, except

                         American National Adult Reasoning Test for estimate of premorbid intelligence

Presurgical history

Patients’ impressions of their current neurological status

 Source:

Clinical Psychology: An Introduction,  Author: Alan Carr

Routledge, Taylor & Francis

 

 

Neuroanesthesia

A close association of Neurosurgeon and neuroanesthesia is mandatory for good clinical outcome of neurosurgical patients. The anesthesia for neurosurgery aincludes anesthesia for surgical procedures for diseases of brain and spine. Neuroanesthesia is different from anesthesia for other surgical procedures. Although any trained anesthetist can pusue a career in the field of neuroanestheasia , there is need to develop acumen of identifying early, minute and subtle changes in the parameters of the neurosurgical patient before, during and after the neurosurgical procedure. In addition,  neuroanesthetist should be prompt to respond to these changes. 
Preanesthetic checkup (PAC) requires anesthetist to be knowledgeable about the common CNS diseases and their possible impact. A knowledge about different surgical approaches, positioning and monitoring of the patient during and after surgery is mandatory for a neuroanesthetist. A neuroanesthetist is not just a passive observer of the surgery but is a important team member who actively coordinates the entire process of anesthesia care. Neuroanesthesist knows how the surgical procedure is being carried out. The neuroanesthetist’s  approach should not be antagonistic to the surgeon but should complement the effort of the neurosurgeon.

Neuroanesthetist should have a vision about the entire neurosurgical procedure so the involvement of neuroanesthetist begings much before the start of actual neurosurgical procedure. So, somebody decides to become neuroanethetist it seems that person has decided to be team person and ready to contribute to patient’s care without being in limelight. Neuroanesthesist plans the positioning, mode of intubation, induction & maintenance of anesthesia, taking care of co-morbidities in a patient , and foresees the unexpected complications.
Prevention of possible positioning injuries during the lengthy neurosurgical procedure should be done before draping of the patient. Care of pressure over the orbits, covering of the eyes and exposure to cornea, pressure over the peripheral nerves, should always be done

Neuranesthetist needs to make extra effort during surgery for degenerative spine, Transoral odontoidectomy, transnasal transsphenoidal surgery, awake craniotomy, sitting position, elective hyperventilation, pediatric neurosurgery , functional neurosurgery and many other neurosurgical procedures. Neuroanesthetist should speculate and take necessary steps for anticipated blood loss, vasospasm, brain retarction, brain edema during  surgery. Cerebral protection during neurosurgery should be the priority of the neuroanesthetist.

Some basic facts: 

Intracranial Pressure (ICP), Cerbral Perfusion Pressure  (CPP), Cerebral Blood Flow (CBF), Cerebral Metaboloc Rate of Oxygen Consumption ( CMRO₂) are important parameters which are modified by blood pressure (BP0, jugular venous pressure (JVP),  Partial pressure of arterial carbon di-oxide or arterial CO2 tension (PaCO2), Hematocrit, blood Glucose level, elevation of the head of the patient, intravascular volume.  

Blood pressure determines CPP. Neuroanesthetist manipulates CPP according to patient’s needs. CPP is reduced when neurosurgeon is working on an aneurysm, or increased during cross clamping to enhance collateral circulation. The measurement of BP by arterial line is most accurate and it should be calibrated at the external auditory meatus to most closely reflect ICP.  So, all neuroanesthetists should be able to put intrarterial line prior to neurosurgical procedures where strict monitoring of BP is mandatory. Common stites of intraarterial line in neurosurgery is the Dorsalis Pedis Artery over the dorsum of the foot. This intrarterial line is removed after neurosurgical procedure is over.

Jugular venous pressue (JVP) also influences intracranial pressure (ICP).

Quickenstedt  established the range of normal ICP and demonstrated the effect of changes in body position and respiration . Lundberg, in 1960, described the 3 ICP waveforms.
Cranium is like a rigid bony sphere with a constant intracranial volume and it contains three components

1. Brain    1400 mL

2. CSF       150 mL

3. Blood    150 mL

Therefore, any change in the volume of the brain causes a reciprocal change in the volume of other intracranial components, i.e., either blood or CSF.  This is the basis of Monro-Kellie hypothesis introduced in neurosurgery by Cushing.

There is a relationship between  intracarnial volume and intracranial pressure.  Because cranium  is  a rigid and non-distensible structure, any increase in the volume of a component would be accompanied by a reciprocal decrease in the volume of the other two components. Once the volume buffering capacity is exhausted, the ICP would begin to rise.

During gradual expansion of a mass lesion, the volume displaced may be CSF, intravascular blood or brain tissue water. Of the three components, CSF appears to be the main buffer and is the first to be displaced as evident  by compressed ventricles  and obliterarted subarachnoid spaces.

The rate of expansion of an intracranial mass is also important. A rapidly growing intracranial mass lesion may outpace the compensatory shift of CSF and even the smallest increase in mass could produce a life threatening increase in ICP. Thus, a large hematoma could be accommodated within a few hours without dangerous rise in ICP.

Intracranial hypertension can lead to secondary changes by interfering with the cerebral blood flow ( CBF). The normal  cerebral blood flow ( CBF) is about 50 mL/100 gram of brain/min.

Cerebral Perfusion Pressure ( CPP) is defined as the difference between mean arterial pressure

( MAP) and intranial pressure (ICP).

CPP= MAP-ICP

Normal range of ICP in an adult is less than 10-15 mmHg.

Cerebral perfusion pressure is normal till the autoregulation mechanism of brain is intact. But there is a range upto which level body is able to maintain CPP.  Between 60 to 160 mmHg of mean arterial pressure brain will be able to receive blood with normal perfusion. But, if MAP falls blow 50 mmHg, features of cerebral ischemia will appear.
Mean Arterial Pressure ( MAP)= Diastolic Pressure+1/3rd of Pulse Pressure 
Pulse pressure= Systolic blood pressure - Diastolic pressure
So, in a normal person MAP = 80 mmHg+ (120mmHg-80mmHg)/3
MAP= 80+40/3
So on average, roughly MAP is about 90-95.

A rise in ICP would lead to a fall in CPP unless buffered by a compensatory rise in blood pressure ( Cushing response). Raised ICP can cause hypertension, bradycardia and respiratory changes. Therefore any patient who is suspected as a case of intracranial space occupying lesion ( ICSOL), like brain tumor or hematoma or granuloma or abscess and complaining of headache, vomiting, blurring of vision then blood pressure and pulse rate should always be monitored. In clinical setting bradycardia is a reliable indicator of rise in ICP in a patient who was otherwise allright sometimes back. Bradycardia is a sign of raised ICP and can precede and appears before deterioration of conscious level ( Drowsinees, disorientation or poor Glasgow Coma Scale) and papillary asymmetry.

Lundberg described three pressure waves namely A waves, B waves and  C waves .

A waves
A waves are pathological  and indicate rapid rise in ICP  for variable period and then rapid fall to the baseline.
The A waves that persist for longer periods( usually 5-20 minutes) are called plateau waves.
Smaller A waves termed “ atypical” or “ truncated” A waves , that often do not exceed an elevation of 50 mm Hg, are also clinically important early indicators of neurological deterioration.

The A waves are accompanied by clinical features  of raised ICP, like headache, vomiting, decerebrate posturing, papillary changes, bradycardia and hypertension and respond to CSF drainage, hyperventilation and osmotic diuretics.

B waves

Occur at the rate of 0.2-2 per minute and are related to respiration.

B waves may be vasomotor in origin. Lundberg initially described them in patients with intracranial hypertension, though they can occur in normal individuals.
B waves are said to be one of the best predictors of outcome after surgery for normal pressure hydrocephalus.

C waves

C waves are low amplitude with afrequency of 4-8 per minute. These waves are thought to be related to Traube-Hering- Mayer waves.
C waves are of little clinical significance.

There is pressure equilibrium in the skull  but if pressure rises then a part of brain herniates. The herniations are subfalcine, tentorial, and tonsillar. In subfalcine herniation, a part of the frontal lobe herniates below the falx to the opposite side . In tentorial herniation ( Uncal herniation) a part of the medial temporal lobe herniated below through an opening in the tent and compresses over the midbrain. In tonsillar herniation, a part of cerebellum,i.e, Cerebellar Tonsil herniates down through the Foramen Magnum and compresses the medulla oblongata ( Coning). Brain Herniation is life threatening as it causes  brain stem compression which contains vasomotor center. Patient presents with drowsiness, decerebrate posturing, papillary asymmetry, bradycardia, hypertension and respiratory irregularities.

Increased ICP is indicated by a sustained elevation in pressure above 15 mmHg or when intermittent A or B waves are recorded.

The normal CSF pressure measured through the lumbar route ranges from 50 to 200 mm H₂O in the lateral decubitus position.

ICP and CPP monitoring are important in the management of head injury patients, especially in whom the decision to operate is equivocal. Surgery may be required if ICP is progressively rising and not responding to conservative treatment with cerebral decongestants. ICP monitoring may also be required in patients of spontaneous subarachnoid hemorrhage (SAH) to assess the effect of cerebral vasospasm and in patients of arrested hydrocephalus and  normal pressure hydrocephalus to take decision about CSF diversion procedure.

Various methods of monitoring the ICP

1.       Intraventricular catheters like External Ventricular Drainage ( EVD): Most accurate, lower cost, also allows therapeutic drainage of CSF

2.       Intraparenchymal catheters (eg. Camino labsor Honeywell/Phillips)

3.       Epidural catheters ( e.g. Fibreoptic tipped catheter: Ladd fireoptic)

4.       Subarachnoid bolt (screw)

5.       Subdural ( eg. Cordis Cup catheter)

Monitoring Systems can broadly be divided into Fluid coupled system and Non-fluid cupled system

In fluid-coupled system a fluid filled catheter or a hollow bolt placed in the ventricle, subarachnoid space or the subdural space connected to a pressure transducer through a fluid-filled line. The transducer converts the hydraulic pressure into an electrical signal which can be displayed  digitally or an oscilloscope.

In Non-fluid coupled systems, the transducer is mounted on the monitoring device itself.

In infants and in children below 18 months of age , the anterior fontanelle is open. Tense anterior fontanelle indicates raised ICP and intraventricular pressure. CSF drainage can be done from the right side lateral angle of the diamond shaped anterior fontanelle.

In clinical setting  cerebral edema is one of the important causes of raised ICP.  if a patient presents with clinical features of raised intracranial pressure, then following steps may be helpful:

Bed rest  reduces the cerebral  metaboloic  rate of oxygen consumption and decreased blood supply

Oxygenation

Elevation of head end of the bed to 30^o

Acetazolamide ( Diamox tablet) is a carbonic anhydrase inhibitor and is available in tablet form . In an adult 250 mg tablet can be given orally three times a day( tds)

Frusemide or Furusemide ( Lasix) is a loop diuretic and is available in both oral and injectable form. A dose of 40 mg twice a day reduces the cerebral edema ICP. But Frusemide use may cause  potassium  loss leading to hypokalemia so serum electrolyte monitoring should also be done. To avoid hypokalemia , potassium supplement is advised for example syp Potklor  1 TSF twice a day or Injection KCL  in Intravenous  infusion may be given. Another drug can be prescribed is Spironolactone( Lasilactone), a potassium sparing diuretic and then potassium supplementation is not required.

Injection Mannitol 100 ml stat or 100 ml 8 hourly ( 1 -1.5 Gm/ kg body weight in divided doses in an adult) for three days and then Syp Glycerol 6 TSF three times a day for about 2 weeks.

Dexamethasone 4 mg 6 hourly in injectabe or oral form. Ranitidine or other antacid should be prescribed alog with steroid to avoid gastritis. Dexamethasone is diabetogenic and raises blood sugar level. Prolong  use is associated with fluid retention and swelling over face and body.

CSF drainage is another way to reduce ICP. Ventricular tap is done usually through the point just anterior to the coronal suture on right side , about 3 cm lateral to the sagittal suture . This is a ethod of reducing ICP in a patient with post meningitic hydrocephalus and at the time of surgery. And if CSF pressure is persistently high then External ventricular drainage system can be used.

Elective hyperventilation is a mode or reducing ICP. Hyperventilation leads to CO₂ wash out which  causes vasoconstriction and decreased blood supply to the brain leading to decreased ICP. In this procedure patient is intubated after giving muscle relaxant and put on ventilation for about 48 hours. The ventilator mode is Controlled Mechanical Ventilation ( CMV) the respiratory rate is low,i.e., about 16/minute and monitoring of the patient is done with arterial blood gases(ABG) in which the pCO₂ is about 25mm Hg ( Normal range of arterial partial pressure of Carbon Dioxide ranges from 25mm Hg to 42 mmHg). Elective hyperventilation is often advise in patients with severe head injury, diffuse axonal injury, in a patient of spontaneous subarachnoid hemorhhage ( SAH) presenting with features of vasospasm, after a prolonged surgery with brain swelling during surgery.

Some surgical ways of reducing ICP are CSF diversion procedures ,  decompressive craniectomy or excision of the intracranial space occupying lesion( ICSOL) like hematoma, tumor or abscess.

Arterial CO₂ tension (PaCo₂ ) is the most potent cerebral vasodilator and it should optimally be about 30-35. Hyperventilation reduces PaCo₂ ( Hypocapnea) which decreases CBV but also CBF. The goal is ideally  end tidal CO₂ ( ETCO2)  of 25-30 mm Hg.

Cerebral Metaboloc Rate of Oxygen Consumption (CMR02) is very important can in simple way it can be explained as the metabolic rate of the brain tissue. So, if hypothermia is induced, the brain tissue metabolism will fall and CMR02  will decrease.  CMRO2 is also reduced with certain neuroprotective agents. Hypothermia, Phenobarbitone decrease CMRO2 and reduce the harmful effects of ischemia.

Average cerebral blood flow (CBF) in an adult is approximately 50 mL/100 gram of brain per minute.
Auto-regulation is the ability of brain to maintain a constant blood flow over a range of perfusion pressure. Thus, CBF is constant between mean arterial pressure (MAP) of 50-150 mmHg.

Hematocrit or Packed Cell Volume ( PCV)  in neurosurgery is critical to balance oxygen carrying capacity (decreased by anemia). If the haematocrit is less which means less haemoglobin in the RBC , so more will flow to brain will be required to maintain oxygen supply to the brain and it will increase the intracranial pressure. It is one of the reason of headache I patients with anemia.

Patient temperature : mild hypothermia provides some protection against ischemia by reducing  CMRO₂ by approximately 7% for each 1^o C drop.

Head end elevation to 30 degree is good for reducing ICP. It facilitates venous return. Some surgeons use head end elevation to 30 degree as a routine but some use the flat end of upper part of OT table and opt for increase in head end elevation if there is need to reduce ICP or control of bleeding during surgery.

Inhalation agents reduce cerebral metabolism except nitrous oxide. They cause vasodilatation and increase cerebral blood volume (CBV) and ICP. And after 2 hours increase CSF which further increases ICP. Most agents increase the CO₂ reactivity of cerebral blood vessels. 
The solubility of nitrous oxide ( N20) is 34 times that of nitrogen. When N₂O comes out of solution in an airtight space it can increase the pressure which may convert pneumocephalus to “ tension pneumocephalus”. It may also aggravate air embolism. Thus caution must be used especially in the sitting position where significant post-op pneumocephalus and air embolism are common. The risk of tension pneumocephalus may be reduced by filling the cavity with fluid in conjunction with turning off N₂O about 10 minutes prior to completion of dural closure.

Halogenated agents ( Isoflurane, desflurane, sevoflurane) suppress EEG activity and provide some degree of cerebral protection. Isoflurane can produce isoelectric EEG without metabolic toxicity. Desflurane, a cerebral vasodilator, increases CBF & ICP, decreases CMRO₂ which tends to cause compensatory vasoconstriction. Sevoflurane increases CBP and ICP and reduces CMRO_{2 .} Mild negative inotrope, cardiac output not as well managed as with isoflurane or desflurane.

Intravenous agents :
Propofol is used for induction & infusion during TIVA ( total intravenous anesthesia). Propofol causes dose dependent decrease in MAP & ICP.  It is more rapidly cleared than thiopental.

Barbiturates ( thiopental) reduce CMRO₂ and scavenge free radicals.   Barbiturates produce dose dependent EEG suppression. Myocardial suppression & peripheral vasodilatation  can cause hypotension and can compromise CPP, especially in hypovolemic patients.

Etomidate, a carboxylated imidazole derivative. It is anesthetic & amnestic. Sometimes produces myoclonic activity which may be confused with seizures. It impairs renal function & should be avoided in patients with renal disease as it may produce renal insufficiency.

Ketamine, a NMDA receptor antagonist, produces dissociative anesthesia,. It may slightly increase heart rate & BP. As ketamine increases intracranial procedure,  ketamine is used less in neurosurgery as compared to short general surgical procedures in general surgery. 

Narcotics in Anesthesia

All narcotics cause dose dependent respiratory depression which can result in hypercarbia and concomitant increased ICP in non-ventilated patients.  Narcotics often contribute to post-operative nausea & vomiting (PONV).

Morphine
Meperidine ( Demerol)
Synthetic narcotics: Remifentanil, fentanyl, Sufentanil, Alfentanil
           Fentanyl crosses the blood brain barrier (BBB), reduces CMRO2, CBV, and so the intracranial pressure ( ICP). It is very commonly used drug in neurosurgery. It may be given as bolus and also as infusion.
           

Some other common drugs used in neuroanesthesia:

Benzodiazepines ( GABA agonists), decrease CMRO₂, anticonvulsant action, produce amnesia.

Lidocaine
Esmolol

Dexmedetomidate: alpha 2 adrenergic receptor agonist, used for control of hypertension post operativelyality of awake craniotomy, either alone or with propofol. Also used to help patient tolerate endotracheal tube without sedatives/ narcotics to facilitate extubation.

Paralytics ( Neuromuscular blocking agents) for Intubation: to facilitate tracheal intubation, should be guided by neuromuscular twitch monitoring. Succinylcholine, rocuronium, vecuronium ( Norcuron), cisatracurium.

Intraoperative evoked potential monitoring
SSEP

Malignant hyperthermia

Malignant hyperthermia is a hypermetabolic state of skeletal muscle due to idiopathic block of Ca⁺⁺ re-entry  into sarcoplasmic reticulum. Transmitted by multifactorail genetic predisposition. Total body oxygen consumption increases by 2 to 3 times.

Incidence 1/15000 in peds, 1 in 40,000 anesthetic administrations in adults. 50% had previous anesthesia without MH. Requently associated with administration of halogenated inhalational agents and the use of sucinylcholline ( fulminant form: muscle rigidity almost immediately after sucinylcholline, may invole masseters leading to difficulty in intubation).

Initial attack and recrudescence may occur post-op . 30% mortality.

Earliest sign increase in end-tidal pCO_2, tachycardia or arrhythmia, DIC ( bleeding from surgical wound or body orifices), ABG ( metabolic acidosis), pulmonary edema, hyperthermia ( temp 44^oC) at rate of 1^o C/ 5 min, limb muscle rigidity, rhabdomyolysis ( increased CPK & myoglobin).

Terminal features are hypotension, bradycardia, and cardiac arrest.

Treatment: Eliminate offending agents ( stop the operation, discontinue inhalation agent and change tubing on anesthesia machine),

 Dantrolene sodium ( Dantrium) 2.5 mg/kg IV infusion till symptoms subside , upto 10 mg/kg

Hyperventilation with 100% oxygen

Surface and cavity cooling: IV, in wound, per NG , PR

Bicarbonate 1-2 mEq/kg for acidosis

IV insulin and glucose to lower K⁺, glucose acts as energy substrate

Procainamide for arrhythmia

Dieresis: volume loading and osmotic diuretic

Prevention: identification of patient at risk ( 4 cm muscle biopsy, abnormal contracture to caffeine or halothane), family history ( any relative), masseter response to succinycholine

Avoid  succinycholine, use non- halogenated anesthetic in patients at risk

Prophylactic oral dantrolene: 4-8 mg/kg/day for1-2 days ( last dose 2 hours before surgery)

How to interpret ABG ( arterial Blood Gases)? Easy!

pH less than 7 is acidic and more than 7 is alkaline.

To understand ABG you should know that normal pH of blood  is 7.40 plus or minus 0.04 ( So, In a normal person blood pH range is 7.36 to 7.44)

Normal range of partial pressure of the dissolved Carbon dioxide in arterial blood pCO₂  is 25 mm Hg to 42 mm Hg. If a person hyperventilates then CO₂ is washed out of the lungs and pCO₂ falls, and on the contrary,  if a person’s respiratory hate is low, then there is CO₂ retention and pCO₂ rises.

ABG is very important investigation for neuroanesthetist and neurosurgeon. Because cerebral blood flow (CBF) , intracranial pressure ( ICP) and cerebral perfusion pressure ( CPP) are directly affected by pCO₂. Dissolved in CO₂ blood is the most potent stimulus for the control of respiratory rate and vasodilatation. If pCO₂ rises the respiratory rate increases and there is cerebral vasodilatation and increase in CBF, CPP and ICP.

But neurosurgeons and neuroanesthetists are concerned about ICP and try to have optimum CBF, CPP and ICP. So, the respiratory rate should be appropriate. If respiratory rate is increased then CO₂ washout from the lungs occur, pCO₂ falls, vasoconstriction occurs and CBF and ICP is decreased. This is the principle and aim of elective hyperventilation , i.e., to reduce ICP by keeping pCO₂ around and 25 mmHg (close to lower side of the normal range). This is a common practice for managing  patients with severe brain edema. But, if there is further reduction in pCO₂ below 25 , then there may be vasoconstriction and brain ischemia. So, Monitoring of the patient on ventilator should be done with ABG, and accordingly the respiratory rate may be modified.

First check arterial pH, if pH is below 7.4 then it is acidosis and if pH is more than 7.4 then patient is having alkalosis.

If acidotic then check pCO_2, if it is more than 40 mmHg then it is due to hypoventilation and patient is having Respiratory Acidosis. But if pCO_2,  is less than 40 mmHg then it is metabolic acidosis and if anion gap is normal ( 8-12 meq/L) then diarrhea may be a cause of Metabolic Acidosis. If anion gap is increased , then renal failure, Lactic acidosis, diabetic ketoacidosis may be the cause of metabolic acidosis.

As mentioned earlier, if pH is more than 7.4 then patient is having alkalosis, which could either be due to respiratory or metabolic cause. So, check for pCO₂, if it is less than 40 then patient may be hyperventilating and pCO2 washout is the cause and it is called Respiratory Alkalosis. Or, if patients pCO₂ is more than 40 mmHg, then alkalosis is due to a metabolic cause and vomiting or diuretic use is  a common cause and is known as Metabolic Alkalosis.

Neurocritical care

The major challenges for the neuroanesthetists is not only limited to operation theatre but role is extended to neurosurgeical intensive care unit, where some issues are frequently encountered, like Hyponatremia
SIADH
Diabetes Insipidus
Pulmonary edema
Hypertension
Sedation
Elective hyperventilation

Commonest complaint at the time of intracranial neurosurgical intervention : Bulging brain
Commonest challenge in post-operative period: Raised ICP & deterioration of conscious level  due to raised Intra cranial pressure.
          Adequate brain relaxation facilitates neurosurgery and reduces the need for excessive brain retraction. Prolong and recessive brain reduces the blood supply to that particular ischemia which causes ischemia and which , in turn, increases brain edema. Sometimes, due to excessive brain swelling surgery is stopped and it becomes difficult to close the dura. So, enough precautions should be taken to avoid this situation. Cool temperature in the operation in the operation theatre is good for the patient.  Other measures include smooth intubation, proper positioning, padding of the pressure points, mild head end elevation, normal neck position to ensure proper venous drainage. Controlled ventilation with slight hypocapnia with target PaCO2 mm Hg induces cerebral vasoconstriction which consequently reduces brain edema.  So, continuous controlled ventilation without any interruption is mandatory during intracranial neurosurgery. Awakening of the patient or light anesthesia allowing movement of the patient, coughing & bucking  on the endotracheal tube create havoc during neurosurgery. This is very common complaint by any neurosurgeon. Excessive rotation at the neck during positioning may hamper venous return. Proper position of the pad below chest and pelvis ensures breathing movement, intrathoracic pressure and venous return and ICP.  Hyperventilation, head end elevation, Dexamethasone, Frusemide and intravenous Mannitol help in reducing brain edema.

  

Sources:

1. Handbook of Neurosurgery. Mark S. Greenberg, 7^th Ed, Thieme, 2010
2. Ramamurthi & Tandon's Manual of Neurosurgery. Tandon PN, Ramamurthy R, Jain PKN, Jaypee Brothers medical Publishers
3. Chapter 6. Intra-operative monitoring written by Babu KS, Rajsekhar VRamamurthy & Tandon’s manual of Neurosurgery ,  Editors:  PN Tandon, Ravi Ramamurthy, Pradeep Kumar Jain N, first edition: 2014 ISBN 978-93-5152-192-1