Role of Neurosurgery

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Learning objectives

  • Role of Surgery for Ischaemic stroke
  • Malignant MCA syndrome and hemicraniectomy
  • Acute Hydrocephalus diagnosis and surgical management
  • Evidence base for selection
  • Appropriateness of referrals


The role of neurosurgery has become more clearly defined by an accumulation of evidence over the years such that surgery for supratentorial bleeds is becoming increasingly uncommon. A more defined use for surgery is in decompressive procedures for ischaemic strokes. The neurosurgical management of Aneurysmal SAH and subdural haemorrhage (technically not stroke as extra-axial) are a significant proportion of neurosurgical workload and each is discussed under their specific articles. Neurosurgery is underpinned by the box principle. The skull is a box within which lies the soft structure of the brain. Anything that causes trauma to the box or its contents will cause an increase in volume of the brain which if left unchecked can lead to progressive damage, dysfunction and ultimately death. Neurosurgery attempts to find ways to relieve the increased intracranial pressure before permanent damage can be done, or to limit any permanent damage to the minimum. These principles underpin neurosurgical management of stroke and its complications. Make that sure you have read the basic chapter on Munro-Kellie hypothesis.

Malignant MCA syndromes and Decompressive Hemicraniectomy

Decompressive hemicraniectomy with durotomy is a procedure first pioneered by Harvey Cushing the famous Boston neurosurgeon in 1905 [Cushing H 1905]. It did not come into usage for stroke until 1956. It has had several uses over the years but it is more so being used now for those with complete occlusion of the distal internal carotid artery or proximal (M1) of the middle cerebral artery. Malignant MCA infarction is seen in about 10% of infarcts and the patient presents with a severe hemiparesis, gaze palsy with eyes deviated away from the side with the weakness and hemisensory loss. Consciousness may be impaired possibly due to raising Intracranial pressure. There will be severe aphasia or neglect depending on the side affected.

  • There is a concern that operating on those with dominant hemisphere malignant MCA syndromes may lead to poor outcome with aphasia and hemiparetic patients. However this has been challenged and each case must be judged individually.
  • There is progressive oedema due to a break down in the blood brain barrier and this tends to peak at approximately 48 hours post stroke. This can lead to transtentorial herniation and death. Needless to say the prognosis is poor and disability in survivors likely to be severe.
  • A small number of studies have shown that removal of the skull on the affected side and allowing herniation of the brain can reduce ICP and can reduce mortality by about 35-50%. Early intervention within the first 24 hours appears to be better. Therefore in a DGH setting these patients need screened and identified early and plans made to move possibly to their stroke unit for joint stroke physician and neurosurgical consultation.
  • The procedure involves bone removal which reduces the ICP by about 15% but then in addition to this the dura is incised and this reduces ICP by 70%. Strokectomy that is the incision and removal of infarcted brain is generally not advocated with the concern that penumbra may be being removed. A large skin flap is fashioned. Bone is removed. The skull flap can be retained and used later in the plastic reconstruction of the wound some weeks or months later [Samandouras G.2011] Until that is done there is an obvious skull defect and the brain covered only by soft tissue remains vulnerable to injury.
  • A post mortem study showed that this was more common in the young, females, those with no prior history of stroke, an abnormal ipsilateral circle of Willis, an increased heart weight and those with carotid occlusion. [Jaramillo et al. 2006]. Various other imaging techniques including DWI.
  • Perfusion studies have all been used to try and identify patients at risk. Serum markers are under study and these include Plasma cellular fibronectin and Serum S100B which are signs of cellular injury. In practice however CT or MRI if available acutely are the main investigations.

Current Selection Criteria

  • These vary from centre to centre and local guidance will be needed. RCP guidance suggest the following should be considered
  • Aged 60 years or younger
  • Clinical deficits suggestive of infarction in the territory of the middle cerebral artery
  • NIHSS of above 15.
  • Decrease in the level of consciousness to give a score of 1 or more on item 1a of the NIHSS
  • Signs on CT of an infarct of at least 50% of the middle cerebral artery territory, with or without additional infarction in the territory of the anterior or posterior cerebral artery on the same side, or infarct volume greater than 145 cm3 as shown on diffusion-weighted MRI
  • Malignant MCA territory infarction is not a contraindication to intravenous thrombolysis. Intravenous thrombolysis is not a contraindication to hemicraniectomy.

Evidence base

  • The evidence base for hemicraniectomy is based on several small studies. The DECIMAL trial [Vahedi K et al. 2007] was randomised and looked at surgery in patients aged 18 to 55 and their subsequent modified rankin score. The trial was stopped after 38 patients were enrolled as there was a 52.8% reduction in death in the treated group. The DESTINY trial [2007] was randomised and controlled and was again able to show a significant reduction in mortality post surgery despite only 32 patients being included. The HAMLET [Hofmeijer J 2009] study again looked at surgery and included 64 patients and showed benefits in mortality up to 48 hours but not beyond. These were the three European surgery trials and on their data was pooled [Vahedi K et al. 2007].
  • The Cochrane database states : Surgical decompression lowers the risk of death and death or severe disability defined as mRS>4 in selected patients < 60 years of age or younger with a massive hemispheric infarction and oedema. Optimum criteria for patient selection and for timing of decompressive surgery are yet to be defined. Since survival may be at the expense of substantial disability, surgery should be the treatment of choice only when it can be assumed, based on their preferences, that it is in the best interest of patients. Since all the trials were stopped early, an overestimation of the effect size cannot be excluded. [Cruz-Flores S et al. 2012]
  • My own experience is that the very small number of young patients who I have referred and had surgery that outcome was surprisingly good and patients have returned to almost complete functional independence. Patient selection is key. Hemicraniectomy is clearly aggressive therapy and may not be appropriate for many patients and families.

Posterior Fossa Infarcts and malignant Cerebellar Infarction

  • Cerebellar infarcts can cause swelling and increased pressure within the posterior fossa leading to compression of the IVth ventricle and hydrocephalus - so call "cerebellar apoplexy" or malignant Cerebellar Infarction. Imaging may show loss of the basal cisterns and brainstem compression. Deteriorating patients with a falling GCS can benefit from surgical management [Mohsenipour I et al. 1999].
  • Suboccipital Decompressive Craniectomy is a safe procedure in patients with malignant cerebellar infarction. Infarct- but not procedure-related early mortality is substantial. Long-term outcome in survivors is acceptable, particularly in the absence of brain stem infarction.
  • Developing symptomatic hydrocephalus should be considered for external ventricular drainage (EVD) or less commonly by ventriculo-peritoneal shunting. Upward herniation is always a risk. A failure of EVD in managing hydrocephalus or ongoing brainstem compression can necessitate suboccipital decompressive craniectomy. Discuss with neurosurgeons early particularly in younger patients with a good baseline.

Acute Hydrocephalus

Cerebrospinal fluid physiology

CSF is formed from the choroid plexuses in the lateral (70%), third (5%) and fourth (5%) ventricles and ependymal cells(20%) lining the ventricles. The epithelium of the choroid plexus forms a barrier between blood and CSF filtering out various substances. CSF Flow is from the lateral ventricles through the foramen of Munro into the third ventricle and then through the aqueduct of Sylvius into the fourth ventricle. The aqueduct is only 2 mm in diameter and is a common site of CSF flow blockage. From there it drains through one of three foramina either laterally through the foramina of Luschka (lateral) or the medially placed foramen of Magendie. CSF then enters the subarachnoid space. It is finally absorbed by the arachnoid villi into the venous sinuses. Obstruction at the level of the aqueduct causes a non-communicating hydrocephalus. Obstruction to CSF flow at the level of the arachnoid villi causes a communicating hydrocephalus. Lumbar puncture is not contraindicated, in fact, it may be diagnostic as well as therapeutic in those with a communicating hydrocephalus where pressures are freely transmitted through the subarachnoid space. CSF is produced by the action of the Na+/K+ ATPase pump actively moving Na+ ions into the lumen of the ventricles which is then followed by H20. This happens in the cuboidal cell epithelial cells that form the choroid plexus. The choroid plexus releases about 500 ml of CSF per day into a volume of 100-150 ml. The choroid plexus selectively filters the CSF so that its content differs from plasma. CSF has a lower glucose, very much lower protein, low urea and a low amino acids content. CSF protein is 1/1000th that of CSF. CSF means that the brain basically floats such that the effective weight of the brain is reduced from 1400 g to about 50 g. The CSF also plays a role in the continual drainage of the ventricular cavities and subarachnoid space. The CSF is replaced three times per day and enough is produced in 3 days to fill the entire brain free skull volume. It is no surprise that acute hydrocephalus can be an acutely fatal event if unrecognised and untreated. Membranes The brain itself is surrounded by 3 membranes sandwiched between it and the skull periosteum. Hydrocephalus is the description of excess CSF. It is usually due to an obstruction within the ventricular system or within the channels in the subarachnoid space that allows CSF to be reabsorbed. Untreated it can lead to raised intracranial pressure. CFS acts as a cushion protecting the brain and the brain floats within it. The total volume of CSF is 150 mls. The daily production is 550 ml/day. The entire CSF replaces itself 3 to 4 times per day. The normal intracerebral pressure (ICP) is 5 to 15 mmHg. The rate of formation of CSF is constant and is not affected by ICP. Absorption of CSF increases linearly as pressure rises above about 7 cms H2O pressure. At a pressure of about 11cms H2O, the rate of secretion and absorption are equal.

Types of Hydrocephalus

Hydrocephalus is divided into communicating where the ventricles are in communication with the subarachnoid space and non-communicating where this is obstructed. In stroke we more commonly see obstructive hydrocephalus when swelling obstructs the aqueduct or the IVth ventricle. This then leads to a rise in ICP and potential brainstem herniation. Up to 20% of those with subarachnoid haemorrhage will develop hydrocephalus usually within the first 3-5 days. This is seen more when there is a large bleed with intraventricular bleeding or perimesencephalic haemorrhage.


Headache, dyspraxia, seizures, nausea, vomiting, eye signs and eventually coma and even death. If hydrocephalus is suspected the diagnosis is made using urgent CT scanning which will help to guide the cause and location of the obstruction.

Foramen of Monro Occlusion of the foramen of Monro is an unusual cause of obstruction of CSF flow. Congenital atresia or stenosis of the foramen of Monro is quite rare. Tumours, blood and oedema and other mass lesions and colloid cyst may grow to such a size that they occlude one or both of the foramina.
Aqueduct of Sylvius Aqueductal stenosis is a congenital malformation. Tumours, blood and localised oedema can cause obstruction. Dilation of ventricles above.
Outlet foramina of the fourth ventricle (Luschka and Magendie) The inability of CSF to exit the fourth ventricle usually results from a posterior fossa tumour, blood or oedema that occludes the exit foramina of the fourth ventricle. Severe infections of the CSF pathways can also lead to scarring and obstruction of the outlet foramina of the IVth ventricle.


The key investigation is CT which will show the dilation of the ventricular system. Initially, the first parts of the ventricles to dilate are the temporal horns. This can be seen early on with axial slices from a CT, the temporal horns should come to a point. They appear rounded and this suggests that pressure in the ventricles is raised. A mass lesion or posterior fossa oedema and blood may be seen. A large stroke may result in midline shift and consequent contralateral ventricular dilatation. An acute increased in pressure within the ventricles causes compression of the venous return in the brain parenchyma immediately adjacent to the ventricle. This manifests as periventricular oedema (reduced density), especially the frontal, temporal and occipital horns. This can all be confirmed on MRI if indicated and this can help to determine the level and cause of obstruction.


Initially observation and a wait and see approach may be tried as sometimes the hydrocephalus can settle spontaneously. Some have used Lumbar puncture e.g. removal of up to 20mls of CSF to get a closing CSF pressure of 15 cm H20 if there is no evidence of obstruction within the ventricular system. Where pressure is equally distributed throughout the ventricles and subarachnoid space then the risks of brain herniation are low. With SAH an LP may also help to remove the blood in the CSF space. Remember that it was not that long ago before simple access to CT that SAH was diagnosed by clinical history and Lumbar puncture showing frank blood and then referred for DSA. This management course would be discussed and agreed with the tertiary centre.

Referral to neurosurgeons is warranted to allows rapid shipping of the patient if things get worse. Then, if there is progression then they can make a burr hole and insert a catheter through the brain into one of the lateral ventricles and allow the CSF in the ventricles to drain out. The is called an external ventricular drain. These are usually placed over the right parietal lobe and can easily be seen on CT scan. There are concerns with SAH that suddenly dropping ICP may precipitate more bleeding so CSF pressures should be maintained. Occasionally they can develop ventriculitis.

Hydrocephalus can be seen more so with bleeding into the ventricles or with external compression on the aqueduct due to posterior fossa swelling which can be due to bleeding or infarction. It is also seen after SAH. The main issue in treatment is that early shunting when there is blood and the high protein content of the cerebrospinal fluid (CSF) may block the shunt.

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  • Vahedi K, Vicaut E, Mateo J, et al. Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke 2007; 38:2506. <a href="">link</a>
  • DESTINY II Study Group DESTINY II: Decompressive Surgery for the Treatment of malignant INfarction of the middle cerebral artery II. International Journal of Stroke & 2011 World Stroke Organization Vol 6, February 2011, 79–86
  • Jüttler E, Schwab S, Schmiedek P, et al. Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery (DESTINY): a randomized, controlled trial. Stroke 2007; 38:2518.
  • Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009; 8:326
  • Pfefferkorn T et al. Long-Term Outcome After Suboccipital Decompressive Craniectomy for Malignant Cerebellar Infarction Stroke. 2009;40:3045-3050 <a href="href=">Link</a>