UKMLA and PLAB Exam: Neurology Notes Updated PDF

UKMLA AND PLAB EXAM: NEUROLOGY NOTES UPDATED WWW.MEDREVISIONS.COM ALL YOU NEED TO PASS YOUR EXAM Syringomyelia Overview Syringomyelia is a chronic condition where a uid- lled cavity, or syrinx, forms within the spinal cord. This condition can lead to progressive damage to the spinal cord over time, particularly aﬀecting the central and anterior spinal cord tracts. It is often associated with conditions like Chiari malformations or spinal cord injuries. If the syrinx extends into the brainstem (medulla), it is termed syringobulbia. Key Point: Strongly associated with Arnold-Chiari malformation (Type I), which involves downward displacement of the cerebellar tonsils through the foramen magnum, leading to obstruction of cerebrospinal uid (CSF) ow. Pathophysiology Syrinx Formation: Typically found in the cervical or thoracic spine, the syrinx expands and compresses the surrounding spinal cord tissue. Aﬀected Pathways: ○ Spinothalamic Tract: Disruption of pain and temperature sensation. ○ Anterior Horn Cells: Motor function aﬀected, leading to muscle weakness and wasting. Clinical Features 1. Dissociated Sensory Loss: ○ Spinothalamic sensory loss: This primarily involves the loss of pain and temperature sensation in a "cape-like" distribution over the shoulders, arms, and upper chest. ○ Loss of re exes: Diminished or absent re exes in the upper limbs due to damage to the anterior horn cells. ○ Bilateral upgoing plantar re exes: Indicating involvement of the corticospinal tracts in advanced cases. ○ Light touch, vibration, and position sense: These senses are typically preserved in the early stages but can be aﬀected later as the syrinx expands and involves the dorsal columns. ○ MCQ Tip: In questions mentioning burn marks on the hands without pain, consider syringomyelia, especially if there is a mention of sensory loss in a shawl-like distribution. 2. Motor De cits: ○ Weakness and wasting of the small muscles of the hands due to involvement of the anterior horn cells, leading to a lower motor neuron (LMN) pattern of weakness. ○ As the condition progresses, upper motor neuron (UMN) signs such as hyperre exia and spasticity may develop in the lower limbs if the syrinx expands to involve the corticospinal tracts. ○ MCQ Tip: Syringomyelia should be considered in patients presenting with a combination of upper limb LMN signs and lower limb UMN signs. 3. Other Symptoms: ○ Horner’s syndrome: Characterised by ptosis (drooping eyelid), miosis (constricted pupil), and anhidrosis (lack of sweating) on the aﬀected side, caused by disruption of the sympathetic pathways. ○ Pain, which can be severe and often exacerbated by coughing or straining. Investigation Investigation Details MRI of the Gold Standard for diagnosis. Visualises the syrinx and assesses its extent and Spine any associated abnormalities like Chiari malformation. MCQ Tip: When a patient presents with a combination of motor and sensory disturbances, and syringomyelia is suspected, always choose MRI of the cervical spine as the initial investigation. CT Scan Can be used to evaluate bony abnormalities but is less sensitive than MRI for detecting the syrinx itself. Dynamic MRI Used to assess cerebrospinal uid (CSF) ow, particularly if associated conditions like Chiari malformations are suspected. Management 1. Surgical Intervention: ○ Indicated in symptomatic patients or if the syrinx is enlarging. The goal is to restore normal CSF ow and decompress the syrinx, which may involve procedures such as posterior fossa decompression in Chiari malformations or direct drainage of the syrinx. ○ MCQ Tip: Consider surgery if a patient with syringomyelia presents with progressive neurological de cits. 2. Monitoring: ○ Asymptomatic patients or those with mild symptoms may be monitored with periodic MRI scans to assess the syrinx’s size and progression. ○ MCQ Tip: In stable cases with no signi cant symptoms, monitoring with regular follow-up and MRI is the recommended management approach. Diﬀerential Diagnosis and MCQ Tips Condition Diﬀerentiation MCQ Tip Multiple Sclerosis Episodes of neurological de cits, Look for relapsing-remitting history (MS) often with optic neuritis. Involves a and involvement of the optic nerve, wide range of CNS locations with brainstem, or cerebellum. demyelinating plaques. Amyotrophic Presents with progressive upper ALS presents with mixed UMN and Lateral Sclerosis and lower motor neuron signs but LMN signs without sensory loss, (ALS) typically does not aﬀect sensory diﬀerentiating it from syringomyelia. modalities. Chiari Often associated with Consider Chiari malformation if MRI Malformation syringomyelia, especially type I. reveals downward herniation of the Symptoms include occipital cerebellar tonsils with associated headaches, neck pain, and signs of syrinx. cerebellar dysfunction. Spinal Cord Tumor May mimic syringomyelia with A rapidly progressive neurological similar motor and sensory de cits de cit with back pain should prompt but often presents with back pain consideration of a spinal cord and more rapid progression. tumour. Peripheral Unlike syringomyelia, peripheral When encountering a question about Neuropathy neuropathies usually present with a sensory loss, consider peripheral stocking-glove distribution of neuropathy if the symptoms start sensory loss and aﬀect both pain distally and there is no evidence of and vibration sensation. central spinal cord involvement. Common MCQ Pitfalls and Tips 1. Confusing Syringomyelia with MS or ALS: ○ Pitfall: Syringomyelia typically presents with a dissociated sensory loss (pain and temperature) and motor weakness in a "cape-like" distribution. ○ Tip: Always consider the unique "cape-like" sensory loss when diagnosing. 2. Incorrect Choice of Imaging: ○ Pitfall: Choosing the wrong imaging modality. ○ Tip: Always opt for MRI of the cervical spine when diagnosing syringomyelia. CT or brain MRI may be used in diﬀerent contexts but are not the rst line for syrinx detection. Note: At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management—you need to apply this knowledge in clinical scenarios, and that comes with experience. To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you eﬀiciently cover the entire MLA content map, ensuring focused and eﬀective learning. Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success. Discover what others say about us: What past PLAB 1 Candidates say about MedRevisions Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was 5000+ UKMLA and PLAB 1 Exam style questions Unlimited timed mocks Spaced repetition learning tool And much more Transient Ischaemic Attack (TIA) Overview A transient ischaemic attack (TIA) is de ned as a temporary period of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction. The symptoms of TIA typically last less than 24 hours, most often less than one hour, and completely resolve without residual neurological de cits. TIAs are often warning signs for future strokes, with a signi cant risk within the rst 48 hours. Epidemiology Incidence: ○ TIAs are more common in older adults, particularly those with risk factors for cardiovascular disease Risk Factors: ○ Hypertension ○ Diabetes ○ Hyperlipidemia ○ Smoking ○ Atrial brillation ○ History of ischemic heart disease Pathophysiology TIAs result from the transient occlusion of cerebral or retinal blood vessels, most often due to thromboembolism. Common sources include: Atherosclerotic plaques in the carotid arteries. Cardiac emboli, especially in atrial brillation. Clinical Presentation Symptoms Sudden onset of focal neurological de cits such as: ○ Unilateral weakness or numbness ○ Dysphasia or aphasia ○ Amaurosis fugax (transient monocular blindness) ○ Dizziness or loss of coordination ○ Diplopia or transient visual disturbances Diagnosis Clinical Assessment: Primarily based on history and neurological examination. Imaging: ○ CT Head: Often performed to rule out haemorrhage but may be normal in TIA. ○ MRI: More sensitive than CT in detecting acute ischemic changes, but not always immediately necessary in the emergency setting. ○ Carotid Doppler Ultrasound: Recommended to assess for carotid artery stenosis, a common source of emboli in TIA. ○ CT or MR Angiography: May be used to visualise intracranial and extracranial vessels. ○ Echocardiogram: Indicated if a cardiac source of emboli is suspected, especially in atrial brillation. Diﬀerential Diagnosis and MCQ Tips Condition Key Point MCQ Tip TIA vs Stroke TIA symptoms resolve within 24 hours; Symptom duration is stroke symptoms persist. crucial—resolution within 24 hours suggests TIA. Migraine with Migraine aura progresses over If the patient reports a history of Aura vs TIA minutes; TIA symptoms are abrupt. migraine and the neurological symptoms develop gradually, consider migraine with aura over TIA. Focal Seizures vs Focal seizures can present with similar The presence of postictal confusion TIA symptoms but often include or motor activity might suggest a stereotyped movements or postictal seizure rather than TIA. confusion, which are not seen in TIA. Syncope vs TIA Syncope involves a temporary loss of Look for a history of sudden loss of consciousness due to decreased consciousness, which is more cerebral perfusion, often with a indicative of syncope. prodrome like lightheadedness or sweating, unlike TIA. Peripheral Peripheral vertigo (e.g., benign If vertigo is the only symptom, Vertigo vs TIA paroxysmal positional vertigo) often especially without associated involves isolated dizziness without weakness or speech changes, other neurological symptoms. consider peripheral causes over TIA. Initial Management Immediate Antithrombotic Therapy: ○ Administer aspirin 300 mg immediately unless contraindicated by: Bleeding disorders or ongoing anticoagulant therapy (immediate imaging is required to exclude haemorrhage). If the patient is already on low-dose aspirin, continue the current dose until specialist review. If aspirin is contraindicated, discuss urgent management with a stroke specialist. Referral: ○ Within 24 hours: If the suspected TIA occurred within the last 7 days, an urgent assessment by a specialist stroke physician should be arranged. ○ Within 7 days: If the TIA occurred more than 7 days ago, refer for specialist assessment as soon as possible. ○ Driving: Advise patients not to drive until they have been reviewed by a specialist. Hospital Admission: ○ Patients with a high risk of stroke (e.g., recurrent TIA, atrial brillation, or signi cant carotid stenosis) should be admitted for observation and further investigation. Risk Strati cation: ○ Use the ABCD2 score to stratify the risk of stroke, although NICE guidelines emphasise urgent specialist review over-reliance on this score. Secondary Prevention Antiplatelet Therapy: ○ First-line: Clopidogrel 75 mg daily is recommended as the rst-line antithrombotic for long-term prevention in patients who have experienced a TIA. ○ Second-line: Aspirin 75 mg daily + modi ed-release dipyridamole 200 mg twice daily should be given to patients who cannot tolerate clopidogrel. ○ Dual Antiplatelet Therapy (DAPT): Although not yet standard, the CHANCE study indicated that high-risk TIA patients might bene t from a 90-day course of aspirin + clopidogrel, reducing the stroke rate compared to aspirin alone Statins: ○ High-intensity statin therapy should be initiated for all patients unless contraindicated, aiming for a target LDL cholesterol level below 1.8 mmol/L (100 mg/dL). Antihypertensives: ○ Blood pressure should be aggressively managed to a target of 70%. Aspirin Dosing: ○ 300 mg immediately in acute TIA followed by 75 mg daily or switch to clopidogrel 75 mg daily for long-term prevention. Imaging Prioritization: ○ CT is often used rst to exclude haemorrhage, especially in acute settings, but MRI is more sensitive for early ischemic changes. Note: At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management—you need to apply this knowledge in clinical scenarios, and that comes with experience. To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you eﬀiciently cover the entire MLA content map, ensuring focused and eﬀective learning. Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success. Discover what others say about us: What past PLAB 1 Candidates say about MedRevisions Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was 5000+ UKMLA and PLAB 1 Exam style questions Unlimited timed mocks Spaced repetition learning tool And much more DVLA: Neurological Disorders Overview The Driver and Vehicle Licensing Agency (DVLA) in the UK sets out speci c guidelines for driving with neurological disorders. Medical professionals must be aware of these regulations to provide accurate advice to patients. These guidelines ensure that drivers with neurological conditions are safe to operate vehicles, minimising risks to public safety. It's crucial to understand the responsibilities and legal implications of advising patients about driving restrictions. KEY PRINCIPLES Patient Responsibility: ○ It is primarily the patient's responsibility to inform the DVLA if they have a condition that may aﬀect their driving. However, if a patient refuses to do so, healthcare professionals must notify the DVLA if there is a signi cant risk to public safety. Healthcare Professional Responsibility: ○ If a patient is unable or unwilling to report their condition, it is the duty of the healthcare provider to inform the DVLA, prioritising public safety over patient con dentiality. DVLA GUIDELINES FOR NEUROLOGICAL DISORDERS Epilepsy and Seizures: First Unprovoked or Isolated Seizure: ○ 6 months oﬀ driving if no relevant structural abnormalities on brain imaging and no de nite epileptiform activity on EEG. ○ If conditions are not met, the driving ban increases to 12 months. ○ Patient Action: Must inform the DVLA. Established Epilepsy or Multiple Unprovoked Seizures: ○ Driving may be allowed if the patient has been seizure-free for 12 months. ○ If seizure-free for 5 years, a 'til 70 license can usually be restored. ○ Group 2 Vehicle Drivers: Must be seizure-free for 10 years before applying to have their license reinstated. Provoked Seizure: If a seizure occurs due to a speci c identi able cause (e.g., head injury), the patient may need to stop driving until the cause is treated or removed. Stroke and Transient Ischaemic Attack (TIA): Single TIA: Patients are generally advised not to drive for 1 month and do not need to inform the DVLA unless they have another TIA or have multiple attacks. Stroke: Patients may resume driving after 1 month if they have made a satisfactory clinical recovery. If there are residual neurological de cits that could impair driving, they must inform the DVLA. Dementia: Mild Dementia: Patients may continue to drive if deemed safe by a medical assessment. Regular reviews are required. Advanced Dementia: Patients with signi cant cognitive impairment or poor insight must not drive. If the patient is unable to inform the DVLA, the healthcare provider must do so. Syncope: Simple Faint: No driving restriction. Single Episode Explained and Treated: 4 weeks oﬀ driving. Single Unexplained Episode: 6 months oﬀ driving. Two or More Episodes: 12 months oﬀ driving. Craniotomy: For Meningioma: 1 year oﬀ driving. If the tumour is benign and there is no history of seizures, the license can be reconsidered 6 months after surgery if seizure-free. Pituitary Tumor (Craniotomy): 6 months oﬀ driving; for trans-sphenoidal surgery, driving may resume when there is no residual impairment likely to aﬀect driving safety. Narcolepsy/Cataplexy: Cease driving upon diagnosis. Driving may resume once symptoms are satisfactorily controlled. Chronic Neurological Disorders (e.g., Multiple Sclerosis, Motor Neuron Disease): DVLA must be informed. A PK1 form (application for driving license holders' state of health) should be completed. MCQ TIPS Epilepsy vs. Syncope: ○ Key Point: Syncope often involves brief loss of consciousness with quick recovery, whereas epilepsy involves postictal confusion and prolonged recovery. ○ MCQ Tip: For Group 1 vehicles, patients with syncope must be free of episodes for at least 4 weeks before driving, while epilepsy requires a longer period of being seizure-free. TIA vs. Stroke: ○ Key Point: TIA symptoms resolve within 24 hours without lasting damage, whereas strokes can leave permanent de cits. ○ MCQ Tip: A patient with a single TIA can usually resume driving after 1 month if symptom-free, whereas a stroke may require more extended evaluation based on residual de cits. Dementia: ○ Key Point: Patients with mild dementia may continue driving with regular assessments, but advanced dementia requires immediate cessation of driving. ○ MCQ Tip: If a patient is diagnosed with dementia and continues to drive, it is crucial to determine their cognitive ability through regular assessments. Multiple Sclerosis (MS): ○ Key Point: MS patients may continue to drive if their condition is stable, but they must inform the DVLA if they experience signi cant symptoms aﬀecting their driving ability. ○ MCQ Tip: For MS patients with relapsing-remitting disease, assess their neurological function after each relapse before advising on driving. KEY POINTS AND COMMON CONFUSIONS Epilepsy in Group 2 Drivers: Stricter rules apply; patients must be seizure-free for 10 years before reapplying for their license. Driving Post-Seizure: After a rst seizure, patients must be seizure-free for 6 months before reapplying to the DVLA. Stroke and TIA: For most cases, patients can resume driving after 1 month if they have recovered satisfactorily and have no residual de cits. Dementia: Continuous monitoring and regular assessments are crucial. Patients with advanced dementia should not drive, and healthcare professionals must inform the DVLA if the patient cannot. Note: At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management—you need to apply this knowledge in clinical scenarios, and that comes with experience. To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you eﬀiciently cover the entire MLA content map, ensuring focused and eﬀective learning. Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success. Discover what others say about us: What past PLAB 1 Candidates say about MedRevisions Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was 5000+ UKMLA and PLAB 1 Exam style questions Unlimited timed mocks Spaced repetition learning tool And much more Normal Pressure Hydrocephalus (NPH) Overview Normal Pressure Hydrocephalus (NPH) is a potentially reversible condition characterised by the classic triad of: 1. Gait disturbance (magnetic gait) 2. Urinary incontinence 3. Cognitive impairment (often called "wet, wacky, and wobbly") It is commonly seen in older adults and is caused by an abnormal accumulation of cerebrospinal uid (CSF) in the brain's ventricles, leading to ventricular enlargement without a signi cant increase in intracranial pressure. CAUSES NPH can be categorised as: 1. Idiopathic (Primary) NPH: ○ Most common type ○ Cause of CSF buildup is unknown ○ Linked to age-related changes in CSF absorption 2. Secondary NPH: ○ Caused by an identi able underlying condition that obstructs CSF ow or absorption: Head trauma Subarachnoid hemorrhage Meningitis Brain tumor Prior brain surgery Idiopathic intracranial hypertension EPIDEMIOLOGY Prevalence: More common in individuals over 60 years of age. Gender: Slight male predominance. Risk Factors: Age, history of head trauma, subarachnoid haemorrhage, meningitis, or other conditions aﬀecting CSF dynamics. CLINICAL FEATURES Gait Disturbance: ○ Often, the earliest symptom is described as a "magnetic gait," where the feet seem stuck to the oor. Urinary Incontinence: ○ Starts as urgency or frequency and may progress to overt incontinence. Cognitive Decline: ○ Memory impairment, bradyphrenia (slowness of thought), and apathy often progress more slowly than in Alzheimer's disease. DIAGNOSIS Neuroimaging: ○ MRI/CT Scan: Ventricular enlargement (ventriculomegaly) without signi cant cortical atrophy. Enlarged lateral and third ventricles are typical, with a relatively preserved cortical mantle. ○ Classic Finding: Ventriculomegaly with an absence of signi cant cortical atrophy diﬀerentiates NPH from other types of dementia. Lumbar Puncture (CSF Tap Test): ○ Purpose: Assesses response to CSF removal, aiding in diagnosis and predicting response to shunting. ○ Findings: Typically, normal CSF pressure and normal cell count, protein, and glucose levels. DIFFERENTIAL DIAGNOSIS AND MCQ TIPS Condition Key Diﬀerentiator MCQ Tip Alzheimer’s More prominent early memory loss, If the question describes a patient Disease language diﬀiculties, and visuospatial with signi cant memory loss and de cits than NPH. MRI typically shows language diﬀiculties in the early cortical atrophy, particularly in the stages, along with cortical atrophy temporal lobes. on imaging, think AD. Parkinson’s Resting tremors, bradykinesia, rigidity, Look for the classic motor Disease and postural instability are hallmark symptoms of PD and the absence of features. Cognitive impairment and early prominent cognitive or urinary urinary incontinence are later symptoms. manifestations of PD. Vascular Dementia (VaD) Stepwise decline in cognitive A history of vascular risk factors function, often with focal neurological (hypertension, diabetes, smoking) de cits (e.g., weakness, sensory and a stepwise decline with focal changes) corresponding to areas of neurological signs should raise stroke or ischemic injury. Imaging suspicion for VaD. shows multiple lacunar infarcts or white matter changes. Other Dementias Consider frontotemporal dementia Be aware of the unique features of (FTD) if behavioural changes and diﬀerent dementias and the personality are more prominent than corresponding imaging ndings. memory loss. Lewy body dementia (LBD) can cause visual hallucinations, uctuations in cognition, and parkinsonism. Medication Side Eﬀects Review the patient's medication list If the question mentions a recent for drugs that can cause gait medication change or disturbances, urinary incontinence, or polypharmacy, consider cognitive impairment (e.g., drug-induced causes in the anticholinergics and diﬀerential. benzodiazepines). Subdural Hematoma Often, a history of head trauma, even Inquire about recent falls or head minor. Symptoms can uctuate, with injuries, especially in elderly headache, drowsiness, confusion, and patients with uctuating focal neurological signs. Imaging neurological symptoms and imaging shows a crescent-shaped collection ndings consistent with SDH. of blood. Creutzfeldt-Jakob Disease: Rapidly progressive dementia with myoclonus and speci c EEG changes. KEY POINTS FOR PLAB 1 Symptoms: Triad of gait disturbance, urinary incontinence, and cognitive decline is key to diagnosing NPH. Imaging: Ventriculomegaly without signi cant cortical atrophy on MRI or CT. Management: Ventriculoperitoneal (VP) shunting can signi cantly improve symptoms, especially gait disturbances. MANAGEMENT Initial Management: ○ Symptomatic treatment addressing gait instability, cognitive decline, and urinary incontinence as needed. De nitive Treatment: ○ Ventriculoperitoneal (VP) Shunting: The mainstay of treatment, often leading to improvement in gait and, to a lesser extent, cognitive and urinary symptoms. Follow-Up: ○ Regular monitoring post-shunt placement for complications like shunt malfunction or infection. COMMON CONFUSIONS FOR PLAB 1 Gait Disturbance vs. Parkinsonism: NPH typically has a magnetic gait with minimal arm swing, while Parkinson’s disease features tremors and rigidity. Diﬀerentiating from Dementias: Alzheimer’s and other dementias may present similarly but lack the ventriculomegaly seen in NPH. Imaging Findings: Remember that ventriculomegaly with preserved cortical mantle is typical for NPH, diﬀerentiating it from other causes of dementia. Note: At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management—you need to apply this knowledge in clinical scenarios, and that comes with experience. To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you eﬀiciently cover the entire MLA content map, ensuring focused and eﬀective learning. Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success. Discover what others say about us: What past PLAB 1 Candidates say about MedRevisions Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was 5000+ UKMLA and PLAB 1 Exam style questions Unlimited timed mocks Spaced repetition learning tool And much more Cauda Equina Syndrome (CES) Overview Cauda equina syndrome (CES) is a rare but severe condition caused by compression of the cauda equina, a bundle of nerve roots at the lower end of the spinal cord. This syndrome is a neurosurgical emergency that requires prompt diagnosis and treatment to prevent permanent neurological damage, including paralysis, urinary retention, and loss of bowel control. Epidemiology Aspect Details Incidence Relatively uncommon, 1-3 per 100,000 people/year Age Typically aﬀects adults between 30 and 50 years old Gender No signi cant gender predilection Risk Factors Lumbar Disc Herniation: Most common cause, particularly large central herniations. Spinal Stenosis: Narrowing of the spinal canal that compresses the cauda equina. Trauma: Vertebral fractures or dislocations. Tumors: Spinal metastases or primary spinal tumors. Infections: Epidural abscesses or osteomyelitis. Postoperative Complications: Especially after lumbar spine surgery. In ammatory Conditions: Ankylosing spondylitis. Pathophysiology Cauda equina syndrome occurs when there is signi cant compression of the nerve roots at the cauda equina level, leading to impaired motor and sensory function in the lower limbs and bladder/bowel dysfunction. Compression may result from: Herniated disc Spinal stenosis Tumors Trauma Other space-occupying lesions Clinical Presentation The classic triad of symptoms in CES includes: Severe Lower Back Pain: Often radiating to one or both legs, described as "sciatica." Saddle Anesthesia: Numbness or sensory loss in the perineal region, including the inner thighs and area around the buttocks. Bladder and Bowel Dysfunction: This may present as urinary retention, incontinence, or loss of bowel control. Additional symptoms may include: Lower Limb Weakness: Motor weakness in the lower extremities, often aﬀecting gait and mobility. Sexual Dysfunction: Loss of sexual function due to nerve involvement. Diﬀerential Diagnosis Condition Key Diﬀerentiators Lumbar Disc Unilateral leg pain, no saddle anaesthesia or bowel/bladder Herniation dysfunction. Multiple Sclerosis Bowel/bladder symptoms with additional neurological signs (e.g., optic neuritis). Spinal Cord Involves upper motor neuron signs due to involvement above Compression the cauda equina. Peripheral Neuropathy Common in diabetes, usually lacks acute severe pain or urinary symptoms. Conus Medullaris Similar to CES but with more prominent upper motor neuron Syndrome signs and early bladder dysfunction. Investigation Clinical Examination: Assess for lower limb weakness, saddle anaesthesia, and diminished re exes. Urgent MRI Spine: The gold standard for diagnosing CES, identifying the level of compression, and the underlying cause such as a herniated disc, tumor, or abscess. CT Myelography: An alternative if MRI is contraindicated, though less commonly used. Bladder Scan: To assess for urinary retention if clinical suspicion exists, but should not delay imaging. Management Stage Intervention Details Immediate Surgical The mainstay of treatment is typically within 48 Decompression hours of symptom onset. Steroid Use Corticosteroids may reduce in ammation but are not a substitute for surgery. Preoperative Analgesia Adequate pain control, often with opioids. Bladder Care Catheterisation may be necessary to relieve urinary retention. Postoperative Physiotherapy Rehabilitation to improve mobility and strength. Bladder and Bowel For those with residual dysfunction. Training Psychological Address the emotional impact of the condition Support and its complications. Prognosis Timing of Surgery: Critical in determining outcomes. Delays can lead to permanent neurological de cits. Residual Symptoms: Despite timely surgery, some patients may experience ongoing bladder, bowel, or sexual dysfunction. Rehabilitation: May require long-term physiotherapy and occupational therapy to maximise function and independence. Common MCQ Pitfalls and Tips Diﬀerentiation from Lumbar Disc Herniation: Remember, CES involves saddle anaesthesia bowel/bladder dysfunction and is a surgical emergency. Investigative Choice: MRI is the de nitive investigation. X-rays are not sensitive for CES, and CT is less commonly used unless MRI is contraindicated. Management Priority: Immediate surgical consultation is crucial. Watch out for distractors in MCQs that suggest non-surgical interventions like physiotherapy or delayed imaging. Confounding Symptoms: Be cautious when diﬀerentiating CES from other causes of radicular pain or neurological de cits, such as MS or spinal cord compression, by focusing on the presence of perineal sensory loss and bowel/bladder symptoms. Understanding the Red Flags: Students must be aware of "red ag" symptoms such as saddle anaesthesia, urinary retention, and acute onset of bilateral lower limb weakness, which necessitate urgent referral and management. KEY POINTS FOR PLAB 1 Surgical Emergency: CES is an urgent condition requiring immediate surgical decompression. Red Flags: Bilateral sciatica, saddle anesthesia, and urinary retention are critical signs. Urgent MRI: The investigation of choice to con rm the diagnosis. Early Intervention: Vital for preventing permanent neurological damage. Note: At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management—you need to apply this knowledge in clinical scenarios, and that comes with experience. To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you eﬀiciently cover the entire MLA content map, ensuring focused and eﬀective learning. Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success. Discover what others say about us: What past PLAB 1 Candidates say about MedRevisions Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was 5000+ UKMLA and PLAB 1 Exam style questions Unlimited timed mocks Spaced repetition learning tool And much more Restless Leg Syndrome (RLS) Overview Restless Leg Syndrome (RLS), also known as Willis-Ekbom Disease, is a neurological disorder characterised by an irresistible urge to move the legs, often accompanied by uncomfortable sensations. These symptoms primarily occur during periods of rest or inactivity, particularly in the evening or at night, and are temporarily relieved by movement. The exact aetiology of RLS is not fully understood, but it is believed to involve the dopaminergic pathways in the brain. RLS is often chronic and can signi cantly impact sleep and quality of life. Epidemiology Aspect Details Prevalence Aﬀects about 5-15% of the general population. Age Can occur at any age but is more common in middle-aged and older adults. Gender Women are more commonly aﬀected than men. Clinical Features Symptoms Details Uncontrollable urge to move the The primary symptom of RLS, often described as a need to legs (Akathisia) relieve an uncomfortable sensation. Symptoms predominantly occur Initially aﬀecting night-time, symptoms may progress to at night daytime as the condition worsens. Symptoms worsen with rest The discomfort typically intensi es when the patient is lying down or sitting for extended periods. Paraesthesias Patients often describe these sensations as "crawling," "throbbing," or "itching." Periodic Limb Movements of Involuntary, repetitive movements of the legs during sleep Sleep (PLMS) can disturb both the patient and their bed partner. Temporary relief of symptoms Symptoms are temporarily relieved by activities like walking with movement or stretching. Causes and Associations Cause/Association Details Genetic predisposition Positive family history is noted in around 50% of idiopathic cases. Iron de ciency RLS is often associated with low iron levels, and correcting the anaemia de ciency can improve symptoms. Pregnancy Particularly in the third trimester, symptoms are common and typically resolve postpartum. Uraemia Often seen in patients with chronic kidney disease. Diabetes mellitus Peripheral neuropathy associated with diabetes can increase the risk of RLS. Diagnosis Clinical Diagnosis: Based on the history of symptoms, especially the pattern of symptom relief with movement and exacerbation at rest. Laboratory Tests: Blood tests are useful to exclude iron de ciency anaemia, with serum ferritin levels

UKMLA and PLAB Exam: Neurology Notes Updated PDF

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