Patient Guides
Clear, straightforward guides for patients
Practical articles covering the questions patients ask most often — from understanding your MRI report to what happens during brain surgery.
What happens during brain surgery?
Brain surgery, or craniotomy, is the subject of considerable anxiety for most patients, understandably. This article explains the process in clear, straightforward terms, from the night before to the first days of recovery. **Before surgery** The evening before surgery, you will meet the anaesthetist, who will explain how you will be put to sleep and kept comfortable throughout. You will be asked not to eat or drink for several hours before the procedure. **On the day** On the morning of surgery, you are taken to the operating theatre. After you are asleep under general anaesthesia, a small area of your hair is shaved, we keep this as minimal as possible. The scalp is cleaned with antiseptic, and local anaesthetic is injected to reduce post-operative pain. **The procedure** An incision is made in the scalp. The skin and muscle are reflected, and small burr holes are drilled in the skull. A specialised saw connects these holes, and a piece of bone, called a bone flap, is lifted. This is the craniotomy. The operating microscope is brought in. Using this magnification, I remove the tumour. If the tumour is near a critical area, I may use intraoperative monitoring, stimulating the brain surface while a neurophysiologist observes for responses, mapping safe corridors. **Closing** Once the tumour has been removed, the bone flap is secured with small titanium plates, the muscle and skin are closed with sutures or staples, and a dressing is applied. You wake up in the recovery room. **After surgery** Most patients spend one night in the high-dependency unit for close observation, then move to the ward. You will be up and walking, with assistance, within 24 to 48 hours. NICE guidelines (NG99, 2019) set out the standards for the neurosurgical pathway, including pre-operative preparation, intraoperative care, and post-operative recovery.
Understanding your MRI report
MRI reports are written by radiologists for other doctors, and they can be intimidating. This guide walks through the common terms you will see and explains what they mean in clear, straightforward terms. **What is an MRI?** An MRI, short for magnetic resonance imaging, uses a strong magnetic field and radio waves to create detailed images of the brain and spine. It does not use radiation. NICE guidelines (NG99, 2019) recommend MRI as the standard imaging for brain tumours, and NICE NG12 (2015) supports direct access MRI for patients with suspected brain tumours based on progressive, subacute loss of central neurological function. **How the report is structured** The report typically opens with the clinical indication, why the scan was ordered, followed by the technique used, and then the findings. The findings section is organised by anatomical region. **Common terms explained** Common terms you may see: - **T1-weighted / T2-weighted / FLAIR**: These are different sequences, each showing different tissue characteristics. FLAIR is particularly useful for looking at the brain's white matter. - **With contrast / Gadolinium**: A contrast agent injected through a vein highlights areas where the blood-brain barrier is disrupted, as happens with many tumours, infections, and inflammation. - **Enhancing lesion**: An area that takes up contrast. Many tumours enhance, but so do infections and some benign conditions. - **Mass effect**: The tumour or lesion is pressing on surrounding structures. - **Midline shift**: The central line of the brain has been pushed to one side by a mass. This is a serious finding that requires urgent attention. - **Oedema**: Swelling around a lesion, common with tumours. - **Ischaemic change**: Areas of the brain that have been affected by reduced blood flow, often age-related. **What to do with your report** Always review your scan with your surgeon, who will put the images up on the screen and walk you through them. The report is a starting point for a conversation, not the end of one.
Questions to ask your neurosurgeon
It is normal to feel overwhelmed during a surgical consultation. This list is meant to be printed and brought with you, so you do not have to remember everything in the moment. **Before your consultation** Bring a family member. They will hear things you miss and think of questions you would not. **Questions to ask** 1. **What exactly is the diagnosis?** Ask for the everyday name and the medical name. Write both down. 2. **Why is surgery recommended, and what happens if I wait?** Some tumours can safely be observed. Others need timely intervention. 3. **What is the goal of the surgery, cure, control, or diagnosis?** The answer shapes expectations for everything that follows. 4. **What are the specific risks in my case?** Every patient's anatomy is different. Generic risk statistics are less useful than the risks specific to your tumour's location. 5. **What should I expect immediately after surgery?** Will you wake up in intensive care? How long will you be in hospital? When can family visit? 6. **What is the recovery timeline?** When can you drive? Return to work? Exercise? 7. **Will I need further treatment after surgery?** Radiotherapy? Chemotherapy? Rehabilitation? 8. **How many of these procedures have you done?** It is appropriate to ask. A straightforward question deserves a straightforward answer. 9. **Who will I see for follow-up?** You should know who your point of contact is on the team. **After the consultation** These questions are the starting point. Your surgeon should welcome them, a well-informed patient is a better partner in their own care. NICE shared decision-making guideline (NG197, 2021) recommends that patients be given clear information about treatment options, risks, and what to expect, in a format they can understand.
Recovery after brain surgery
Recovery from brain surgery follows a general pattern, but each patient's experience is unique. This guide describes the typical timeline and what you can do to help your own recovery. **First 24–48 hours** You will likely spend the first night in a high-dependency or intensive care unit, where nurses check your neurological status hourly, pupil reactions, limb strength, level of consciousness. This is standard protocol, not a sign that anything is wrong. You will have a drip for fluids, possibly a drain from the wound, and regular pain relief. Most patients are sitting up in a chair by the second day. **Day 2–5 on the ward** Once stable, you move to a standard ward. Physiotherapists will help you walk. Occupational therapists will assess your safety for discharge. Your stitches or staples typically remain in for seven to ten days. The wound must be kept dry during this period. **First two weeks at home** Fatigue is the universal experience. The brain is healing, and it demands rest. Plan for short periods of gentle activity interspersed with naps. Avoid lifting anything heavier than a kettle. Do not drive, both for medical and legal reasons; typically you must inform the licensing authority and wait for clearance. **Weeks two to six** Energy returns gradually. Most patients on sick leave from desk-based work can return at four to six weeks. Physical jobs may require longer. Light exercise, such as walking, is encouraged from week two. Avoid contact sports and swimming until the wound is fully healed. **Six weeks to three months** This is when many patients begin to feel like themselves again. Follow-up scans are scheduled around this period. Some cognitive fog is normal and usually resolves. If it persists, tell your surgical team. **The most important thing** The single most important thing you can do for your recovery: sleep. The brain heals during deep sleep. Do not feel guilty about resting. NICE guidelines (NG99, 2019) set out the standards for post-operative neurosurgical recovery, including monitoring, mobilisation, and discharge planning.
Living with a brain tumour
For many patients, a brain tumour is not a single event but an ongoing condition that requires long-term management. This guide addresses the practical, day-to-day aspects. **Understanding your tumour** First, understand the specific nature of your tumour. Some are monitored with scans every six to twelve months and require no active treatment. Others need repeated interventions. Knowing which camp you are in helps frame expectations. **Surveillance scans** These are a fact of life. The frequency depends on the tumour grade and behaviour. Treat scan day as a planned day, bring someone with you, have a relaxed afternoon scheduled, and don't make important decisions that day. The emotional response to scan results is real, whether the news is good or uncertain. **Medication** Anti-epileptic drugs are common, even if you have never had a seizure. Take them consistently. Steroids (dexamethasone) may be prescribed to reduce brain swelling. Steroids are powerful and need careful management, never stop them suddenly. **Fatigue management** Brain-tumour-related fatigue is different from ordinary tiredness. It does not always respond to rest. Pacing, planning activity in short blocks with deliberate rest in between, is the most effective strategy. **Driving** Many brain tumour diagnoses require you to inform the Road Transport Department (JPJ). The rules depend on the tumour type and whether you have had a seizure. Your surgeon will advise, but the legal responsibility to inform the authority is yours. **Work** Many patients continue working. Flexibility around scan appointments and periods of treatment is the key requirement. An honest conversation with your employer, supported by a letter from your medical team, usually leads to workable accommodations. **Emotional life** Anxiety about progression, scans, and the future is near-universal. It is not a sign of weakness. Professional psychological support, patient support groups, and open communication with family all help. My team can connect you with a clinical psychologist who specialises in neuro-oncology patients. NICE guidelines (NG99, 2019) set out the standards for living with and beyond a brain tumour, including surveillance protocols, medication management, driving guidance, and psychological support.
What is Gamma Knife radiosurgery?
Gamma Knife radiosurgery is one of the most precise tools in neurosurgery, yet the name often causes confusion. There is no knife and no incision. This guide explains what it is, how it works, and what to expect. Gamma Knife is a form of stereotactic radiosurgery. Stereotactic means three-dimensional targeting. Radiosurgery means a single, high dose of radiation delivered with surgical precision. The Gamma Knife unit contains approximately 200 individual cobalt-60 sources, each producing a narrow beam of gamma radiation. Each beam by itself is too weak to damage tissue. But at the point where all 200 beams converge, the combined dose is concentrated and powerful. Think of it as the opposite of conventional radiotherapy. In conventional radiotherapy, a broad beam is delivered in small daily fractions over several weeks, and normal tissue recovers between sessions. Gamma Knife delivers the entire treatment in a single session, relying on extreme precision rather than fractionation to spare normal tissue. **What conditions can Gamma Knife treat?** Small to medium-sized brain tumours (primary and metastatic), meningiomas, pituitary adenomas, acoustic neuromas, arteriovenous malformations (AVMs), and trigeminal neuralgia. It is also used for residual or recurrent tumour after open surgery, and for patients who cannot safely undergo an operation. **What happens on the day?** You arrive in the morning. A lightweight stereotactic frame is fitted to your head under local anaesthetic, this ensures millimetre accuracy by providing fixed reference points. Some centres now use a frameless system with a custom thermoplastic mask. Either way, the principle is the same: your head must remain perfectly still. You then have a planning MRI or CT scan. While you rest, the team (neurosurgeon, radiation oncologist, and medical physicist) designs your treatment plan. This is the most time-consuming part, and it is where the expertise lies. Every beam is shaped and weighted individually. When the plan is ready, you lie on the treatment couch, the frame or mask is locked into position, and the treatment begins. You feel nothing. Depending on the complexity, treatment lasts between twenty minutes and over an hour. **Afterwards.** The frame or mask is removed, and you go home the same day. Some patients experience a mild headache or fatigue for a day or two. The pin sites heal within a few days. There is no wound care, no stitches, and no restrictions on daily activity beyond common sense for the first twenty-four hours. **Results take time.** Gamma Knife does not remove a tumour on the day. The radiation damages the DNA of the target cells, and the biological effect unfolds over weeks to months. Tumours stop growing, then gradually shrink. Vascular lesions such as AVMs take one to three years to obliterate. Follow-up is with surveillance MRI scans, typically at six months, twelve months, and annually thereafter. **Is it always the right choice?** No. Gamma Knife works best for small, well-defined targets. Lesions larger than about three to four centimetres, those causing significant mass effect, or those requiring a tissue diagnosis usually need open surgery. The decision is made at a multidisciplinary meeting where your specific case is discussed by all the relevant specialists.
Trigeminal Neuralgia — An Update
Trigeminal neuralgia is a disorder characterised by recurrent attacks of severe, unilateral facial pain affecting one or more divisions of the trigeminal nerve. Patients typically describe the pain as electric-shock-like; stabbing, shooting or lancinating; sudden and extremely intense; lasting from a fraction of a second to approximately two minutes; and precipitated by harmless stimuli such as touching the face, speaking, eating, shaving, washing or brushing the teeth. Attacks may occur repeatedly in volleys. Between attacks, many patients are pain-free, although some develop a background aching, burning or continuous discomfort. The mandibular and maxillary divisions (V3 and V2) are affected more commonly than the ophthalmic division (V1). Pain usually remains confined to one side of the face. Bilateral symptoms, particularly when occurring simultaneously, should raise concern for an alternative or secondary diagnosis. **Contemporary classification** 1. Classical trigeminal neuralgia: Occurs when a blood vessel compresses the trigeminal nerve at or near its root entry zone and produces morphological changes such as distortion, displacement or atrophy of the nerve. A vessel merely touching the nerve is not sufficient; clinically relevant neurovascular compression with nerve deformation is more persuasive. 2. Secondary trigeminal neuralgia: Caused by another identifiable disorder such as multiple sclerosis, cerebellopontine-angle or skull-base tumour, epidermoid cyst, arteriovenous malformation, inflammatory or infiltrative disease, or other structural lesions affecting the trigeminal pathway. 3. Idiopathic trigeminal neuralgia: The patient has a convincing TN phenotype, but investigations do not demonstrate significant neurovascular compression or another structural cause. Each category can be subdivided into purely paroxysmal TN or TN with concomitant continuous facial pain. **Why does it occur?** The most widely accepted mechanism is focal damage to the trigeminal nerve's myelin, usually near the root entry zone. This permits abnormal electrical transmission between adjacent nerve fibres (ephaptic transmission) and makes the nerve hyperexcitable. The disorder is therefore not simply "a blood vessel touching a nerve" — many asymptomatic individuals have vascular contact on MRI. The clinically important finding is compression that corresponds to the symptomatic side and causes displacement, indentation or atrophy of the nerve. **Clinical diagnosis** Trigeminal neuralgia is primarily a clinical diagnosis. The history is more important than any single scan. The cardinal features are: recurrent unilateral facial-pain paroxysms; pain confined predominantly to the trigeminal distribution; severe, electric, stabbing, shooting or sharp pain; attacks lasting seconds, occasionally up to about two minutes; attacks triggered by innocuous facial or oral stimulation; and stereotyped attacks that are similar each time. A brief refractory period may follow an attack, during which touching the trigger area does not immediately provoke another paroxysm. Most patients with classical or idiopathic TN have a normal neurological examination. A focused examination should include light touch and pinprick sensation in V1, V2 and V3; corneal reflexes; facial motor function; muscles of mastication; hearing and cerebellar examination; other cranial nerves; oral and dental examination; and examination for cutaneous lesions. Findings that should cause concern include objective facial sensory loss, absent or asymmetrical corneal reflex, facial weakness, hearing loss or other cranial neuropathy, bilateral symptoms, prominent continuous numbness or burning, symptoms beginning at a young age, pain outside the trigeminal distribution, and constitutional, malignant or inflammatory features. **Investigations** MRI brain with a dedicated trigeminal-nerve protocol should form part of the work-up. Recommended imaging combines high-resolution three-dimensional heavily T2-weighted imaging (such as CISS or FIESTA), three-dimensional time-of-flight MR angiography, and contrast-enhanced three-dimensional T1-weighted imaging. A normal MRI does not disprove trigeminal neuralgia. Conversely, vascular contact on MRI does not by itself prove that the vessel is responsible for the pain. Routine blood tests (full blood count, renal profile, sodium, liver function) are relevant before and during pharmacological treatment. **Important differential diagnoses** Not every severe facial pain is trigeminal neuralgia. Conditions that may mimic it include dental disease, temporomandibular disorder, persistent idiopathic facial pain, painful trigeminal neuropathy, post-herpetic neuralgia, glossopharyngeal neuralgia, cluster headache, SUNCT or SUNA, migraine with facial pain, sinus or orbital disease, giant-cell arteritis, and malignancy or skull-base disease. Painful trigeminal neuropathy is typically more continuous, burning or squeezing and is often accompanied by sensory disturbance. **Treatment** Treatment is individualised according to pain severity, age, general health, medication tolerance, MRI findings and patient preference. First-line medical therapy: Carbamazepine and oxcarbazepine remain the principal first-line medications. Carbamazepine has the strongest historical evidence. Oxcarbazepine often has fewer drug interactions and may be better tolerated, although hyponatraemia remains an important concern. Treatment is started at a low dose and titrated according to response and adverse effects. These drugs are taken regularly rather than only during individual attacks. Monitoring includes full blood count, liver function, renal function, serum sodium, medication interactions, and watching for rash, fever or mucosal ulceration. For patients with ancestry from populations in which HLA-B*15:02 is prevalent (including several Asian populations), pharmacogenetic testing should be considered before starting carbamazepine because this allele is strongly associated with Stevens-Johnson syndrome. Other agents include lamotrigine, baclofen, gabapentin, pregabalin, and botulinum toxin type A in selected patients. When should surgery be discussed? A neurosurgical opinion is appropriate when: medication no longer controls the pain; effective doses cause unacceptable adverse effects; medication is medically unsuitable; attacks significantly impair nutrition, speech, sleep or quality of life; the patient wishes to understand definitive treatment options; there is compelling neurovascular compression on MRI; or the diagnosis remains uncertain. Early counselling allows patients to make a considered decision before they become exhausted, malnourished or frightened by recurrent attacks. Microvascular decompression (MVD): Through a small retrosigmoid craniotomy, the trigeminal nerve is inspected and the offending artery or vein is mobilised or separated from the nerve. MVD offers the highest probability of durable pain relief in appropriately selected classical TN, preserves facial sensation in most patients, often produces immediate relief, and avoids deliberately lesioning the nerve. Risks include CSF leak, hearing impairment, facial numbness, vascular injury, cerebellar injury, infection and other uncommon but serious complications. Percutaneous procedures: Radiofrequency thermocoagulation, balloon compression, and glycerol rhizolysis reach the trigeminal ganglion through the foramen ovale. Advantages include relatively short procedures, rapid pain relief, usefulness in elderly or medically frail patients, and repeatability. Limitations: facial numbness is expected to varying degrees, recurrence is more common than after successful MVD, corneal numbness is particularly important when V1 is treated, and dysaesthesia, masseter weakness and rarely anaesthesia dolorosa may occur. Stereotactic radiosurgery (Gamma Knife): Delivers focused radiation to the trigeminal nerve. Advantages: no incision, no passage of a needle through the face, usually performed as a day procedure, useful when open surgery is not ideal. Limitations: pain relief is usually delayed rather than immediate, recurrence may occur, facial numbness may develop, and the treatment effect is less predictable than successful MVD. **Key clinical pearls** 1. Diagnose the phenotype before treating the scan — a vascular loop on MRI is not the diagnosis. 2. "Tooth pain" is not always dental pain — many patients undergo unnecessary dental treatment before TN is recognised. 3. Numbness changes the conversation — objective sensory loss or multiple cranial-nerve abnormalities should prompt reassessment for secondary disease. 4. A normal scan does not exclude TN — MRI supports classification but does not replace clinical judgement. 5. The culprit is compression, not mere contact — the most meaningful findings are indentation, displacement, distortion or atrophy of the nerve. 6. Carbamazepine responsiveness supports but does not prove the diagnosis. 7. Do not wait until the patient is desperate before discussing surgery — patients should understand their options while still able to weigh different trade-offs. 8. Choose the operation for the patient, not merely for the MRI — MVD for durability and preservation of sensation; percutaneous treatment for immediate relief accepting numbness and recurrence; radiosurgery for incision-free treatment accepting delayed response. 9. Continuous pain predicts a more complex outcome — the brief electric-shock component is more predictably relieved than constant background discomfort. 10. The therapeutic goal is not only pain relief — successful treatment should restore eating, speaking, sleep, personal care, confidence and the ability to touch the face without fear.
Understanding Low Back Pain & Sciatica
Low back pain and sciatica are two distinct syndromes that often present together in the same consultation. Low back pain is axial pain centred between the lower ribs and gluteal folds, often mechanical and non-specific. Sciatica is leg-dominant pain from irritation or compression of a lumbosacral nerve root, most commonly L5 or S1, and may include sensory, motor or reflex changes. The first step in any consultation: decide which syndrome you are treating. **The first 90 seconds: sort the patient** Every consultation should begin by sorting the patient into one of three categories. First, danger: cauda equina syndrome, progressive deficit, cancer, infection, or fracture. These demand urgent action. Second, root: dermatomal leg pain, tension signs, and focal neurological change point toward a compressive radiculopathy. Third, mechanical: axial pain, movement-related, with no convincing root deficit. The principle is simple: triage before terminology, urgency before elegance. **Localise clinically before ordering imaging** A focused clinical assessment should precede any scan. The history covers the pain map, provoking factors, function, and bladder, bowel or sexual symptoms. Tension signs include the straight-leg raise and crossed straight-leg raise when appropriate. Motor examination checks L4 (knee extension), L5 (great-toe dorsiflexion), and S1 (plantar flexion). Reflex and sensory testing covers patellar and Achilles reflexes, dermatomal sensation, and the saddle region if indicated. Examine gait, heel walking and toe walking — the patient often reveals the deficit before the couch examination. **Red flags: cauda equina syndrome** The most important diagnosis not to miss is cauda equina syndrome. Do not wait for painless retention. Warning signs include new difficulty initiating or controlling urination, altered urinary sensation or awareness, saddle sensory change, bilateral symptoms, sexual dysfunction, or progressive weakness. These require urgent MRI, urgent spinal review, and documented timing and progression. This is a surgical emergency. **MRI: a clinical question, not a ritual** There is no indication for routine MRI in acute uncomplicated low back pain or sciatica without red flags. MRI is indicated when it will change care: persistent disabling symptoms, intervention planning, or diagnostic uncertainty. Urgent MRI is required for suspected cauda equina syndrome, infection, malignancy, or progressive deficit. When MRI is obtained, demand concordance: the level, side, and root must match the symptoms. A discordant scan does not explain the patient's pain and may lead to unnecessary treatment. **The default treatment is active recovery** For most patients, the default treatment has four components. First, understanding: explain the diagnosis, expected course, and safety net. Second, movement: continue normal activity and avoid prolonged bed rest. Third, rebuild: graded exercise, strength, mobility, and confidence. Fourth, review: track function and neurology, not pain scores alone. Recovery is structured, supported, and reassessed — it is not simply doing nothing. **Match treatment intensity to the problem** Treatment should escalate in proportion to the clinical need. The foundation tier applies to all patients: education, activity, exercise, and addressing sleep, work, and psychosocial barriers. Medicines should be individualised: NSAIDs only when appropriate. Avoid routine gabapentinoids, oral steroids, and benzodiazepines for sciatica — the evidence does not support their routine use. Image-guided epidural injection may be considered for selected cases of acute, severe sciatica, but not for non-specific low back pain. Surgery is reserved for emergency neurology or persistent, concordant radicular symptoms that have not responded to appropriate non-surgical care. **Surgery: the right patient, the right promise** When surgery is discussed, the ideal conversation confirms three things. First, symptoms and neurological findings fit the compressed root. Second, disability is unacceptable despite appropriate care, or urgency demands action. Third, the patient understands the benefits, limitations, and alternatives. A microdiscectomy does best at relieving concordant radicular leg pain. It is less predictable for longstanding numbness, motor recovery, and axial back pain. Never promise a 'new back.' The goal is specific: address the compressed nerve root causing concordant symptoms. **The five rules** 1. Name the syndrome before treating it. 2. Screen for danger every time. 3. Localise clinically before imaging. 4. Use MRI only when it changes management. 5. Treat the patient — not the scan.
Transsphenoidal Resection of a Pituitary Tumour
The pituitary gland is a small gland at the base of the brain that controls many of the body's hormones. A pituitary tumour may affect health by producing excessive hormones, reducing normal pituitary hormone production, or pressing on nearby structures such as the optic nerves. Most pituitary tumours are benign. Transsphenoidal surgery may be recommended when a tumour is pressing on the optic nerves, causing visual loss, producing excessive hormones, or has enlarged significantly. The operation is performed through the nose using an operating microscope, avoiding a conventional skull opening in most patients. This guide explains what to expect before, during and after microscopic transsphenoidal pituitary surgery — from the multidisciplinary team and preoperative assessment through to hormone monitoring, nasal care, recovery, risks, and when to seek urgent medical attention.
Hydrocephalus — Information for Patients, Parents and Families
Hydrocephalus is a condition in which cerebrospinal fluid (CSF) builds up within the ventricles of the brain, placing pressure on the brain and potentially interfering with normal function. It can occur at any age — before birth, during infancy or childhood, in adulthood, or in older adults as normal-pressure hydrocephalus (NPH). Symptoms vary by age and how quickly the pressure develops. Babies may present with a rapidly increasing head size, vomiting, irritability and a tense fontanelle. Older children and adults may develop headache, nausea, visual disturbance, difficulty walking, cognitive changes, and bladder problems. This comprehensive guide covers causes, diagnosis, and both main surgical treatments — endoscopic third ventriculostomy (ETV) and ventriculoperitoneal (VP) shunting — as well as recovery, recognising shunt malfunction or ETV failure, signs of infection, and long-term follow-up.