pressure within the system giving rise to ventriculomegaly and death if not treated.Neurosurgery is the surgical speciality that deals with disease involving the brain and spinal cord. It is a tertiary centre-based speciality located in large teaching hospitals. Neurosurgery can broadly be subdivided into neurovascular, neuro-oncology, skull base, pituitary, functional, paediatric, and spinal.
A bleed within the subdural space as a result of a shearing injury to bridging cortical veins. These occur in the young as a result of severe traumatic brain injury (TBI), are typically acute, and require an emergency craniotomy to evacuate the clot. Elderly patients on anticoagulants may suffer from a chronic collection that presents as a headache or neurological deficit, which is drained with one or two burr holes.
This type of haemorrhage occurs within the subarachnoid space and most commonly is as a result of trauma. Cases you will encounter on the neurosurgical ward will be as a result of a ruptured aneurysm.
TBI remains the commonest cause of death in the under 40s. TBI is a non-specific term describing blunt, penetrating, or blast injuries to the brain. It is further classified into mild, moderate, or severe based on the GCS score. Neurosurgical departments and neurointensive care units look after patients with severe TBI (GCS score <9; mortality is 40%; see Table 36.1).
Table 36.1 Classification of head injury
| Classification | GCS score | Mortality |
| Mild/minor | 13–15 | 0.1% |
| Moderate | 9–12 | 10% |
| Severe | <9 | 40% |
There are a variety of tumours observed within the CNS. It is important to appreciate that there are several classification systems to describe brain tumours (i.e. by location or cell type). In the forebrain and cerebellum, tumours can be thought of as within the brain matter (intra-axial) or outside the brain matter (extra-axial). The most common intra-axial tumours are metastases (breast in females and lung in males).
The ventricular system within the brain plays a central role in the production (choroid plexus) and transport of CSF. In adults there is 150 mL of CSF produced at a rate of 20 mL/hour.
Therefore, any obstruction to flow and/or failure to absorb CSF will result in pressure within the system giving rise to ventriculomegaly and death if not treated.
This is a neurosurgical emergency. It is a clinical syndrome resulting from compression of the spinal roots (cauda equina). It presents with pain (sciatica), paraesthesia/anaesthesia in the sacral distribution (saddle), urinary retention or incontinence, and/or faecal incontinence. The most likely cause of CES is a prolapsed lumbar intervertebral disc. Appreciate that emergency surgery for decompression is required within 24 hours of the onset of urinary or faecal symptoms to preserve some sphincteric function.
Refers to any disease of the spinal column that results from the ageing process (i.e. wear and tear) that occurs to the bone and soft tissues of the spine. This is observed in the cervical spine (termed cervical spondylomyelopathy) and most commonly affects levels C5/6, C6/7, and C7/T1 as well as in the lumbar spine affecting levels L4/5 and L5/S1 most frequently. You should develop an understanding of the anatomy of the spine, the relation of the nerves to the surrounding structures, and tie this in with dermatomes/myotomes so that you may correlate clinical signs with anatomy.
This is a pressure transducer placed within the subdural space or brain parenchyma to measure ICP (normally 5–15 mmHg) in the unconscious patient with a severe TBI.
This is a catheter placed into the frontal horn of the lateral ventricle in the non-dominant hemisphere and is used to divert CSF flow in patients with acute hydrocephalus or a severe TBI in which a rising ICP needs controlling.
This is a diagnostic procedure which involves the insertion of a spinal needle into the spinal subdural space both to measure the CSF pressure (in communicating hydrocephalus) and to sample the CSF (diagnosis of SAH and meningitis).
Burr hole drainage of acute-on-chronic subdural haematoma (ACSDH), image-guided biopsy of tumour, decompressive craniectomy, anterior cervical discectomy, and laminectomy.
The patients you may see in clinic can be broken down in to either cranial or spinal. The most commonly observed cranial cases in clinic are those that broadly fall into neurovascular conditions, brain tumours, and disorders of CSF flow. Spinal cases are either degenerative or spinal tumours.
Intracranial vascular disorders can be broadly categorized into (1) cerebral aneurysms, (2) arteriovenous malformations (AVMs), and (3) cavernomas.
These are out-pouching of the tunica interna and media through deficient external layers of arterial bifurcations within the circle of Willis. When they rupture they result in bleeding within the subarachnoid space and are classified according to anterior or posterior circulation. Size is observed on digital subtraction angiography (DSA). Incidental unruptured aneurysms are followed up after coiling or clipping.
AVMs are congenitally dilated communications between the arterial system and the venous system without intervening capillaries. Present with haemorrhage, seizures, or neurological dysfunction. Around 80% of AVMs will have haemorrhaged by the age of 50 years but the average age of diagnosis is ~33 years with an annual risk of bleeding of 2–4% per year. They can be diagnosed on CT, MRI, and DSA. It must be noted that 10% of AVMs will be associated with a cerebral aneurysm.
These are bundles of sinusoidal capillaries with no arterial supply or venous drainage. They are low-flow, low-pressure vascular malformations with a propensity to haemorrhage. Present with seizures, progressive neurological deficit, ± haemorrhage. These lesions are not seen on angiography but can be seen on MRI and CT with a popcorn appearance. Depending on their location, these lesions can be resected if they are giving rise to intractable seizures or a neurological deficit secondary to repeated haemorrhage (0.25–0.75% yearly risk).
The commonest brain tumour is a secondary (i.e. metastasis). The commonest primary brain tumours are of glial origin called gliomas. The WHO grade gliomas as follows:
• 1 = astrocytomas—commonest primary brain tumour occurring between the ages of 40–60 years with 2:1 male:female ratio.
• 2 = diffuse astrocytoma—occurring in younger adults with a mean age of 30 years.
• 3 = anaplastic astrocytoma—mean age of presentation 40–50 years. These lesions have a tendency to progress to grade 4 tumours.
• 4 = astrocytoma—glioblastoma multiforme represents 55% of all astrocytomas in between ages of 50–70 years. They can be primary (i.e. tumours that occur de novo) or secondary (i.e. tumours that were initially low grade and progressed).
All cases are discussed in the neuro-oncology MDT. Diagnosis is made by an image-guided biopsy of the lesion. If the lesion is clearly a high-grade lesion then a craniotomy and resection of tumour may be undertaken without prior tissue biopsy. Intraoperative tissue samples are taken and sent to the neuropathology laboratory as a ‘frozen section’ to confirm the histological diagnosis. Higher grades (rather expectedly) have a poorer prognosis despite complete resection and adjuvant treatment.
The disturbance of CSF formation, flow, or absorption 
an in the volume occupied by this fluid in the nervous system is called hydrocephalus. One essential concept that you must appreciate when trying to understand pathologies of CSF flow is the Monro–Kellie doctrine. The doctrine states that as the volume of the cranium is fixed, any expansion of either of its constituents (i.e. blood, CSF, and brain tissue) must be compensated for by the remaining constituents to maintain a state of equilibrium. Hence any expansion of either CSF volume (e.g. through failure of absorption or obstruction of flow) or blood (through haemorrhage) will result in compression of the brain parenchyma. After this compensatory mechanism (e.g. reductions in the venous and CSF volumes) is exhausted, brain parenchyma will be compressed from rising ICP inevitable neurological compromise.
This is ventriculomegaly secondary to an obstruction of CSF flow between the ventricles, which are characteristically over-expanded on imaging. This is typically caused by compression of the system from the outside (i.e. within the surrounding brain parenchyma) by bleeds, tumours, or by intraventricular lesions. CSF flow diversion can be either through an external ventricular drain, endoscopic third ventriculostomy, or insertion of a ventriculoperitoneal shunt.
This is ventriculomegaly that results from failure of CSF absorption by the arachnoid villi. The absorption process is hindered by CNS infection, during and soon after SAH and high protein states. There is free communication between the different ventricular compartments so use an external ventricular drain, serial LPs, or a ventriculoperitoneal shunt if persistent.
Spinal neurosurgery can be broken down into (1) degenerative disease, (2) tumours, (3) infection, and (4) haemorrhage.
The level of the disc protrusion is identified by the myotomes and dermatomes affected.
Typically causes neck pain, radicular symptoms (pain along a dermatomal distribution as a result of compression/irritation of the nerve root), and myelopathy (weakness along a specific myotome secondary to cord compression). A large central disc herniation will compress the cord and a ‘myelopathic picture’ such as spasticity and limb weakness. A lateral disc protrusion will compress the exiting nerve root leading to radicular symptoms that are typically pain, numbness, weakness, and paraesthesia. Cervical myelopathy is managed via an anterior (i.e. anterior cervical discectomy and fusion) or a posterior (cervical laminectomy) decompression.
This is characterized either by root compression (i.e. sciatica = radiculopathy) or canal stenosis. Spinal stenosis neurogenic claudication that occurs during walking and or standing. Flexing the hips, bending forward, or sitting down relieves the pain. Neurogenic claudication is unlike arterial claudication, which can occur at rest. Another distinguishing factor is the presence of arterial pulses in neurogenic claudicants, so remember to examine for peripheral pulses. Treatments are analgesia, nerve root injections, and surgical (i.e. removing the offending disc (discectomies) or decompression (laminectomy)).
Tumours affecting the spine are classified by their anatomical location. Extradural tumours are commonly located close to the vertebral bone from which they receive their blood supply. Intradural intramedullary tumours are those arising from the spinal cord parenchyma. (See Fig. 36.1.)
Fig. 36.1 Classification of spinal tumours.
The management of all spinal tumours is centred on three important tenets:
It is critical to decompress the spinal cord to prevent further neurological deterioration and obtain a tissue diagnosis to determine appropriate post-resection therapy. Treatment option for metastasis is radiotherapy, but most intradural extramedullary lesions are benign and do not need more than surgical resection. Intradural intramedullary lesions are surgically resected and patients undergo postoperative radiotherapy.
The neurosurgical team are an essential part of the on-call trauma team. After Airway, Breathing, and Circulation have been stabilized, Disability (i.e. level of consciousness) needs to be assessed. This is best done using the universally accepted Glasgow Coma Scale (GCS).
The GCS was developed to facilitate concise and reproducible assessment of the level of consciousness of a patient, which would in turn allow for effective communication regarding that patient between all members of the medical team. The score for the scale is out of 15, with 3 denoting coma or death. It must be remembered that you cannot score <3 (considered a major faux pas). Patients scoring 8 or less are considered at imminent risk of airway compromise and need urgent anaesthetic assessment with a view to being intubated, ventilated, and sedated. Patients with a neurological cause for a low GCS need hourly neuro-observations. (See Table 36.2.)
Table 36.2 Glasgow Coma Scale
| Eyes (E) | Verbal (V) | Motor (M) |
| 1. No eye opening | 1. Makes no sounds | 1. No movements |
| 2. Opens eyes to painful stimuli | 2. Incomprehensible sounds | 2. Extensor posturing |
| 3. Opens eyes to voice | 3. Inappropriate words | 3. Flexor posturing |
| 4. Opens eyes spontaneously | 4. Confused, disorientated | 4. Move limb away from pain |
| 5. Oriented, converses normally | 5. Moves limb towards pain | |
| 6. Obeys command | ||
| (This reflects the AVPU scale too) | T. If the patient is intubated |
There are around 20,000 cases of major trauma in the UK per year, which result in over 5000 deaths. Up to 80% of these patients will have sustained a TBI. These cases will present to the ED where they will be rapidly assessed using the ATLS® protocol. Following stabilization of their airway, breathing, and circulation a CT brain scan will be performed as part of the radiographic trauma series. Neurological signs can be easily documented using the ASIA (American Spinal Injury Association) chart.
• Diffuse axonal injury with loss of grey–white differentiation.
• Arise as a result of an injury to the middle meningeal artery (derived from the external carotid artery) as it courses behind the pterion—the bony junction between the frontal, parietal, temporal, and sphenoid bones.
• Typically, the patient sustains a blow to the side of the head without suffering a deterioration in level of consciousness at the time (defined as the lucid period) and then has a sudden drop in GCS score.
• Depending on the size and degree of mass effect, an urgent surgical evacuation via a craniotomy may be warranted.
• Results from injury to pial bloods vessels.
• It is normally observed over the surface of the brain, (i.e. the convexity), and is managed conservatively, but one must be careful when taking the history from these patients to make sure that an aneurysmal bleed did not give rise to a collapse and a subsequent TBI.
• Find out about any regular anticoagulants/antiplatelet therapy. These only the risk of bleeding after trauma but not before a traumatic episode. (See Fig. 36.2.)
Fig. 36.2 Types of brain haemorrhage. EDH, extradural haematoma; SDH, subdural haematoma. Reproduced with permission from Richard Graham and Ferdia Gallagher, Emergencies in Clinical Radiology, 2009, Oxford University Press.
• In addition to injury to the brain parenchyma, accompanying bony injuries to the calvarium (skull) are also common.
• Skull base fractures are another subset of bony injuries. They can result in a CSF leak (rhinorrhoea and otorrhoea). These patients may have periorbital (panda eyes) and retromastoid (Battle sign) bruising. Samples of fluid leaking from their nose or ears need to be sent for beta-transferrin (biochemical marker specific to CSF) testing in the biochemistry laboratory. Pneumovax is needed as a prophylaxis.
• If the CSF leak does not settle, they may need a surgical repair of the dural defect that has resulted from the skull base fracture.
• Any evidence of air locules within the brain parenchyma (pneumocephalus) on (an ideally fine-cut) CT brain scan should signify that there is likely either a skull base fracture or compromise of an air-containing sinus (i.e. frontal, sphenoid, or ethmoid sinus).
Honours
Cushing response refers to the compensatory mechanisms that the brain undertakes to compensate for rising ICP (secondary to a change in one of the components described in the Monro–Kellie doctrine). Early signs of rising ICP are decreased or decreasing GCS, agitation, and confusion. As ICP rises even more, the patient will start to vomit in the absence of nausea secondary to medullary compression. Cardiac monitoring may also demonstrate new-onset arrhythmias. As coma develops, the patient may only have reflexive responses to painful stimuli which may subsequently disappear. Once the brainstem has herniated the patient will have cardiorespiratory arrest.
Cushing’s triad is made up of three signs that are observed: hypertension, bradycardia, and apnoea.
• At the most severe end of the TBI spectrum there are two radiographic observations that demonstrate that the injury has been so severe that no neurosurgical intervention would alter the outcome.
• Severe displacement (in relation to the Monro–Kellie doctrine) of the brain parenchyma results in migration of the brainstem through the foramen magnum, better known as ‘coning’. This is a terminal event that is characterized by the Cushing response.
• Diffuse axonal injury with loss of grey–white matter differentiation is observed when either the brain has endured a severe acceleration–deceleration injury or when the brain has had a prolonged period of hypoxia due to neurovascular or cardiopulmonary compromise.
• Both these radiological findings are catastrophic and are terminal/unsurvivable.
• Annual estimated rate of 6–8 per 100,000 in the Western world.
• Up to 15% of patients die before they reach medical care.
• aSAH has a mortality of 10% in the first few days and almost 50% in the first 2 weeks. The peak age of presentation is between 55–60 years of age and 30% of bleeds occur during sleep.
• Classically patients complain of a sudden-onset, worst-ever headache in 97% of cases (‘the worst headache in my life’, ‘being kicked at the back of the head’ or a ‘thunderclap headache’).
• Up to 60% of patients may have a preceding (‘sentinel’) headache of lessor severity or shorter duration.
• Patients may complain of symptoms of meningism (i.e. neck stiffness, N&V, photophobia and visual disturbance (double vision ± ptosis)).
• They may be admitted to the ED unconscious or in a coma.
• Following a concise history taking and a thorough neurological examination, a non-contrast CT brain scan is performed urgently.
• If the patient is scanned within 48 hours of the headache the blood appears as an area of high density (like bone-white) within the subarachnoid space. The blood may also extend into the ventricles (intraventricular haemorrhage).
• If the CT brain scan is inconclusive, a LP is performed 12 hours after the onset of the headache. If the red cell count in serial bottles (i.e. xanthochromia) and the bilirubin is above the threshold in these samples then a diagnosis of SAH is made. Xanthochromia, a yellow discolouration of CSF due to breakdown pigment is indicative of SAH.
• Upon diagnosis, THE patient is started on nimodipine (A calcium channel blocker). The patient is then admitted to the neurosurgical ward and will undergo a CT-guided catheter cerebral angiogram to identify and further define an aneurysm.
• A decision is then made whether the aneurysm can be treated endovascularly or neurosurgically via clipping.
The clinical condition arising from dysfunction of multiple lumbar and sacral nerve roots within the spinal canal as a result of compression of the cauda equina (L2 to sacrum and Latin for horse’s tail). Compression may occur from disc herniation, spondylosis, trauma, local neoplasm, or abscess. It is a relatively uncommon condition and represents only 0.4% in those presenting with low back pain. Up to 90% of proven cases of CES will have experienced urinary retention at some point along their course, and anal sphincter tone is reduced in 60–80% of cases. Saddle anaesthesia is the most commonly observed sensory disturbance. Weakness along more than one nerve root is also common. Patients will often present with SPINE:
Patients may complain of longstanding unilateral sciatica that has become bilateral. Male erectile dysfunction is a late feature. Patients with CES have variable time courses that can be broken down into three groups. Take a clear history from all patients with low back pain associated with sphincteric dysfunction in the ED to identify CES:
• First group have sudden-onset symptoms of CES with no previous history of back symptoms.
• Second group have a longstanding history of recurrent low back pain and sciatica.
• Third group present with low back pain and bilateral sciatica.
All cases of suspected CES need an urgent MRI and be booked for surgical decompression on the next-day operative list if confirmed.
You should develop an understanding of the more commonly performed procedures. These are typically those procedures that are performed in an emergency to prevent further and irreversible neurological deficits. The layers you need to know about are SCALP:
• Pericranium (cranium brain matter).
• The drainage of acute-on-chronic subdural haematoma (ACSDH) may be achieved by the placement of one or two burr holes through the skull with a dural incision to release the underlying collection.
• Two burr holes are placed either side of the apex of the haematoma.
• Warmed normal saline is then irrigated through both burr holes until the effluent is no longer blood stained.
• The scalp is infiltrated with xylocaine containing adrenaline (epinephrein) (to reduce scalp bleeding).
• Two incisions are placed over the frontal and parietal aspects of the collection.
• Burr holes are fashioned with a handheld electric (if the patient is awake) or a pneumatic drill (if patient is under GA).
• A cruciate incision is then made through the dura.
• If the collection is under high pressure, it will be discharged through the first dural incision.
• Copious wash of the subdural space is performed with normal saline until the effluent is clear.
• A drain is passed from the parietal burr hole into the subdural space.
• This drain is secured and connected to a free drainage bag.
• The scalp is then closed; first the galea with an absorbable suture and then the skin with clips or a non-absorbable suture.
• The patient then returns to the ward and remains on flat bed rest for 24–48 hours.
• The drain is taken out after 24 hours and 4 hours later the patient is started on DVT prophylaxis.
To ask the boss
Recurrence rates following ACSDH drainage are up to 30%. Santarius et al.1 demonstrated through a RCT that the use of a subdural drain more than halved the incidence of ACSDH recurrence at 6 months (9.3% vs 24%). There are, of course, risks involved too.
• Acute SDHs overlie the fronto-temporo-parietal cortex.
• The craniotomy also provides access to the middle meningeal artery, which is the commonest cause of an acute extradural haematoma.
• Both these neurosurgical entities require emergency evacuation when the patient is neurologically compromised or if there is significant mass effect.
• Time is of the essence and once the patient is on the operating table decompression should occur within 10 min and in the absence of unforetold complications the whole procedure should not take more than 60 min ‘skin to skin’.
• The skin is shaved and a large question mark incision is marked out starting just below the zygomatic arch 1 cm in front of the tragus.
• The scalp is incised to the bone with a scalpel and haemostasis is maintained by the application of Raney clips.
• The temporalis muscle is then cut. The scalp flap is reflected and up to four burr holes are fashioned with a handheld drill.
• The burr holes are connected together using a craniotome.
• Using elevators the bone is lifted off the dura.
• If there is an extradural haematoma it is evacuated with copious wash. Any points of bleeding (i.e. middle meningeal artery) are stopped using bipolar diathermy.
• In the presence of an acute SDH, a C-shaped incision is made through the dura and the underlying haematoma is evacuated.
• Once the clot has been evacuated, the dural defect is closed using continuous sutures and the bone flap is secured to the skull using bioplates and screws.
• The scalp is then closed in a layered manner (galea first with an absorbable suture and subsequently metallic clips to skin).
• Spinal decompression can either be anterior or posterior.
• Anterior approaches are typically performed on the cervical spine, although they can be performed in all other parts of the vertebral column, and involve the removal of one or two discs with implantation of an artificial disc, and are sometimes reinforced by metalwork.
• Posterior approaches can be performed in all segments of the vertebral column. Most commonly a laminectomy is performed.
• A midline incision is made along the avascular aponeurosis.
• Intraoperative radiography is used to accurately locate the correct site.
• Dissection down the midline is performed using monopolar diathermy until the spinous processes are reached.
• The musculature is reflected off the midline laterally until the lateral extent of the laminae is observed bilaterally.
• Using either a drill or a handheld rongeur the lamina is removed.
• The underlying ligament is removed until the spinal theca is observed. Care is taken not to puncture the dura or injure the exiting nerve roots.
• The wound is then closed in layers with placement of a drain depending on the degree of haemostasis achieved.
Reference
1. Santarius T, Kirkpatrick PJ, Ganesan D, et al. (2009). Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. Lancet 374(9695):1067–73.
During your time on the neurosurgical firm it is critical you master both the neurological examination and the use of the GCS. Take every opportunity given to you both in clinic and on the admissions ward at taking a focused history. Hold back from finding out what the admitting diagnosis is and try to formulate your own differentials.
The most common neurosurgical stations in examinations are usually aSAH or brain tumours. A patient actor may give a history of a sudden-onset, worst-ever headache associated with nausea, vomiting, photophobia, neck stiffness, and possible neurological deficit. The diagnosis should be obvious to you immediately and once you pick up on the cues you will then have ample opportunity to showboat your knowledge of the field by asking more probing questions.
As with all other histories, feel free to use SOCRATES for pain histories. Once you have exhausted this you need to be able to obtain a concise sequence of events in your head and subsequently formulate a series of focused questions that are tailored according to the pathology being discussed. In the case of the sudden-onset headache you need to know:
• when, where, and how it came on
• what they were doing at the time
• have they had something like it before (sentinel headache or regular migraine?)
• was it relieved by simple analgesia (unlikely in aSAH)
• did they develop a neurological deficit (unlikely in migraine) etc.
Ask if your patient suffers from any other medical conditions for which they have seen a doctor. This is a sure-fire way of assuring that you get a comprehensive medical history. Uncontrolled hypertension and the use of anticoagulants for cardiac arrhythmias are of interest to neurosurgeons as they are associated with cerebral haemorrhage.
Your risk of aSAH in the presence of polycystic renal and liver disease and first-degree family members who have suffered an aSAH. All oncological history is of interest as it may mean the patient has a genetic predisposition to cancer.
Is critical as the risk of significant blood loss or uncontrollable haemorrhage is massively when the patient has recently taken anticoagulants such as warfarin, aspirin, and clopidogrel. The exact dates and times need to be identified.
Recent INR needs to be obtained and normalized prior to surgery. Blood products may minimize the risk of intraoperative haemorrhage.
Smoking and the use of illicit drugs such as cocaine your likelihood of suffering a SAH.
Simple things are common, you are unlikely to be presented with a complex neurosurgical case in your exams. In all probability you may be asked to examine a patient’s motor and sensory function. Alternatively, you may be asked to examine a set of cranial nerves looking specifically for a cranial nerve deficit. The eyes are the easiest to examine because ocular deficits are reproducible. The slick use of an ophthalmoscope is essential and you will be expected to be able to identify papilloedema and mention its causes (remember raised ICP links in directly with the Monro–Kellie doctrine so it can only be related to haemorrhage, a space-occupying lesion, and/or a disorder of CSF flow). You need to do this confidently and the only way you can achieve this is to pair up with somebody and pretend to have different scores and assess each other.
• Although you are unlikely to perform a LP during your neurosurgical attachment, you need to make sure you have practised performing a LP in the skills laboratory on a mannequin.
• This needs to be done with a colleague observing and you need to be comfortable talking through the procedure while performing it.
• A central tenet of the procedure is that the spinal cord ends at L1/2 (continuing as the cauda equina below), hence the ideal intervertebral space to aim for is the L3/L4 or L4/5.
• This is easily identified as it is the highest point of the iliac crest and is located on a level with the spinous process of the L4 vertebrae.
• It is important to point your spinal needle rostrally and keep it in the midline.
• The needle will ‘give’ once the dura is breached.
• You will feel three pops as you penetrate the supraspinous, interspinous, and ligamentum flavum ligaments.
• Always attempt to measure the opening and closing pressure (diagnostic tool for communicating hydrocephalus) or at least say that you would as it is likely to score points in an OSCE station.
• Throughout the procedure always check that the patient is comfortable and on completion of the procedure place a dry dressing over the puncture site and instruct the patient to lay flat for at least an hour to reduce the occurrence of a post-LP headache.
• The severity of headache correlates to the size of the puncture so use a pencil-point, small-gauge spinal needle if possible.