Updated for UKMLA and PLAB Exam - Neurology Notes

Syringomyel ia

Over view

Syringomyel ia 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, par ticularly affecting the central and anterior spinal cord tracts. It is often associated with conditions l ike 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 cer vical 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

Cl inical Features

1 Dissociated Sensor y Loss:

○ Spinothalamic sensor y loss: This primarily involves the loss of pain and temperature sensation in a "cape-l ike" distribution over the shoulders, arms, and upper chest

○ Loss of reexes: Diminished or absent reexes in the upper l imbs due to damage to the anterior horn cells

○ Bilateral upgoing plantar reexes: Indicating involvement of the cor ticospinal tracts in advanced cases

○ Light touch, vibration, and position sense: These senses are typically preser ved 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 syringomyel ia, especially if there is a mention of sensor y loss in a shawl-l ike distribution.

2. Motor Decits:

○ 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 hyperreexia and spasticity may develop in the lower l imbs if the syrinx expands to involve the cor ticospinal tracts

○ MCQ Tip: Syringomyel ia should be considered in patients presenting with a combination of upper l imb LMN signs and lower l imb UMN signs.

3 Other Symptoms:

○ Horner ’s syndrome: Characterised by ptosis (drooping eyel id) , 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 Spine Gold Standard for diagnosis. Visual ises the syrinx and assesses its extent and any associated abnormal ities l ike Chiari malformation

MCQ Tip: When a patient presents with a combination of motor and sensor y disturbances, and syringomyel ia is suspected, always choose MRI of the cer vical spine as the initial investigation.

CT Scan Can be used to evaluate bony abnormal ities but is less sensitive than MRI for detecting the syrinx itself.

Dynamic MRI Used to assess cerebrospinal uid (CSF) ow, par ticularly if associated conditions l ike Chiari malformations are suspected

Management

1 . Surgical Inter vention:

○ 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 surger y if a patient with syringomyel ia presents with progressive neurological decits

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 signicant symptoms, monitoring with regular follow-up and MRI is the recommended management approach

Differential Diagnosis and MCQ Tips

Condition

Multiple Sclerosis (MS) Episodes of neurological decits, often with optic neuritis. Involves a wide range of CNS locations with demyel inating plaques

Amyotrophic Lateral Sclerosis (ALS)

Presents with progressive upper and lower motor neuron signs but typically does not affect sensor y modal ities

Chiari Malformation Often associated with syringomyel ia, especially type I. Symptoms include occipital headaches, neck pain, and signs of cerebellar dysfunction

Spinal Cord Tumor May mimic syringomyel ia with similar motor and sensor y decits but often presents with back pain and more rapid progression.

Tip

Look for relapsing -remitting histor y and involvement of the optic ner ve, brainstem, or cerebellum

ALS presents with mixed UMN and LMN signs without sensor y loss, differentiating it from syringomyel ia.

Consider Chiari malformation if MRI reveals downward herniation of the cerebellar tonsils with associated syrinx.

A rapidly progressive neurological decit with back pain should prompt consideration of a spinal cord tumour.

Peripheral Neuropathy

Unl ike syringomyel ia, peripheral neuropathies usually present with a stocking - glove distribution of sensor y loss and affect both pain and vibration sensation

When encountering a question about sensor y loss, consider peripheral neuropathy if the symptoms star t distally and there is no evidence of central spinal cord involvement

Common MCQ Pitfalls and Tips

1 . Confusing Syringomyel ia with MS or ALS:

○ Pitfall: Syringomyel ia typically presents with a dissociated sensor y loss (pain and temperature) and motor weakness in a "cape-l ike" distribution.

○ Tip: Always consider the unique "cape-l ike" sensor y loss when diagnosing

2. Incorrect Choice of Imaging:

○ Pitfall: Choosing the wrong imaging modal ity

○ Tip: Always opt for MRI of the cer vical spine when diagnosing syringomyel ia. CT or brain MRI may be used in different contexts but are not the rst l ine for syrinx detection

Note:

At MedRevisions, we have dedicated years to helping candidates excel in the PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

Transient Ischaemic Attack ( TIA)

Over view

A transient ischaemic attack ( TIA) is dened as a temporar y 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 decits. TIAs are often warning signs for future strokes, with a signicant risk within the rst 48 hours.

Epidemiology

● Incidence:

○ TIAs are more common in older adults, par ticularly those with risk factors for cardiovascular disease

● Risk Factors:

○ Hyper tension

○ Diabetes

○ Hyperl ipidemia

○ Smoking

○ Atrial brillation

○ Histor y of ischemic hear t disease

Pathophysiology

TIAs result from the transient occlusion of cerebral or retinal blood vessels, most often due to thromboembol ism. Common sources include:

● Atherosclerotic plaques in the carotid ar teries.

● Cardiac embol i, especially in atrial brillation.

Cl inical Presentation

● Symptoms Sudden onset of focal neurological decits such as:

○ Unilateral weakness or numbness

○ Dysphasia or aphasia

○ Amaurosis fugax (transient monocular bl indness)

○ Dizziness or loss of coordination

○ Diplopia or transient visual disturbances

Diagnosis

● Cl inical Assessment: Primarily based on histor y and neurological examination

● Imaging:

○ CT Head: Often per formed to rule out haemorrhage but may be normal in TIA.

○ MRI: More sensitive than CT in detecting acute ischemic changes, but not always immediately necessar y in the emergency setting.

○ Carotid Doppler Ultrasound: Recommended to assess for carotid ar ter y stenosis, a common source of embol i in TIA.

○ CT or MR Angiography: May be used to visual ise intracranial and extracranial vessels.

○ Echocardiogram: Indicated if a cardiac source of embol i is suspected, especially in atrial brillation.

Differential Diagnosis and MCQ Tips

Condition

TIA vs Stroke TIA symptoms resolve within 24 hours; stroke symptoms persist Symptom duration is crucial resolution within 24 hours suggests TIA.

Migraine with Aura vs TIA Migraine aura progresses over minutes; TIA symptoms are abrupt

If the patient repor ts a histor y of migraine and the neurological symptoms develop gradually,

Focal Seizures vs TIA Focal seizures can present with similar symptoms but often include stereotyped movements or postictal confusion, which are not seen in TIA.

consider migraine with aura over TIA.

Syncope vs TIA

Syncope involves a temporar y loss of consciousness due to decreased cerebral per fusion, often with a prodrome l ike l ightheadedness or sweating, unl ike TIA

The presence of postictal confusion or motor activity might suggest a seizure rather than TIA.

Look for a histor y of sudden loss of consciousness, which is more indicative of syncope.

Peripheral Ver tigo vs TIA

Peripheral ver tigo (e.g., benign paroxysmal positional ver tigo) often involves isolated dizziness without other neurological symptoms

If ver tigo is the only symptom, especially without associated weakness or speech changes, 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 special ist review.

■ If aspirin is contraindicated, discuss urgent management with a stroke special ist .

● Referral:

○ Within 24 hours: If the suspected TIA occurred within the last 7 days, an urgent assessment by a special ist stroke physician should be arranged

○ Within 7 days: If the TIA occurred more than 7 days ago, refer for special ist assessment as soon as possible.

○ Driving: Advise patients not to drive until they have been reviewed by a special ist .

● Hospital Admission:

○ Patients with a high risk of stroke (e.g., recurrent TIA, atrial brillation, or signicant carotid stenosis) should be admitted for obser vation and fur ther investigation

● Risk Stratication:

○ Use the ABCD2 score to stratify the risk of stroke, although NICE guidel ines emphasise urgent special ist review over-rel iance on this score.

Secondar y Prevention

● Antiplatelet Therapy:

○ First-l ine: Clopidogrel 75 mg daily is recommended as the rst-l ine antithrombotic for long -term prevention in patients who have experienced a TIA.

○ Second-l ine: Aspirin 75 mg daily + modied-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 benet 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)

● Antihyper tensives:

○ Blood pressure should be aggressively managed to a target of <130/80 mmHg.

● Anticoagulation:

○ If atrial brillation is present , long -term anticoagulation with war farin or a direct oral anticoagulant (DOAC) is indicated to reduce stroke risk.

Investigations

● Blood Tests:

○ FBC, U&Es, fasting glucose, l ipid prole, and coagulation studies should be per formed.

● ECG:

○ To identify atrial brillation or other cardiac abnormal ities

● Echocardiogram:

○ Especially if there is a suspicion of a cardiac source of embol i

Common Confusions

● TIA vs. Stroke:

○ Remember that TIA symptoms completely resolve within 24 hours, while stroke symptoms persist beyond this period. Stroke may also be accompanied by imaging evidence of infarction.

● Management of TIA vs. Stroke:

○ In the acute setting of TIA, immediate antiplatelet therapy is crucial, whereas in stroke, thrombolysis or thrombectomy may be considered if within the therapeutic window.

● Carotid Ar ter y Stenosis:

○ Carotid Doppler should be per formed to assess for signicant stenosis Carotid endar terectomy is considered for patients with stenosis >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 PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

DVL A: Neurological Disorders

Over view

The Driver and Vehicle Licensing Agency (DVL A) in the UK sets out specic guidel ines for driving with neurological disorders. Medical professionals must be aware of these regulations to provide accurate advice to patients These guidel ines ensure that drivers with neurological conditions are safe to operate vehicles, minimising risks to publ ic safety It's crucial to understand the responsibil ities and legal impl ications of advising patients about driving restrictions.

KEY PRINCIPLES

● Patient Responsibil ity:

○ It is primarily the patient's responsibil ity to inform the DVL A if they have a condition that may affect their driving However, if a patient refuses to do so, healthcare professionals must notify the DVL A if there is a signicant risk to publ ic safety.

● Healthcare Professional Responsibil ity:

○ If a patient is unable or unwill ing to repor t their condition, it is the duty of the healthcare provider to inform the DVL A, prioritising publ ic safety over patient condential ity

DVL A GUIDELINES FOR NEUROLOGICAL DISORDERS

Epilepsy and Seizures:

● First Unprovoked or Isolated Seizure:

○ 6 months off driving if no relevant structural abnormal ities on brain imaging and no denite epileptiform activity on EEG

○ If conditions are not met , the driving ban increases to 12 months.

○ Patient Action: Must inform the DVL A.

● Establ ished 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 l icense can usually be restored.

○ Group 2 Vehicle Drivers: Must be seizure-free for 10 years before applying to have their l icense reinstated.

● Provoked Seizure: If a seizure occurs due to a specic identiable cause (e.g., head injur y) , 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 DVL A unless they have another TIA or have multiple attacks.

● Stroke: Patients may resume driving after 1 month if they have made a satisfactor y cl inical recover y. If there are residual neurological decits that could impair driving, they must inform the DVL A

Dementia:

● Mild Dementia: Patients may continue to drive if deemed safe by a medical assessment Regular reviews are required.

● Advanced Dementia: Patients with signicant cognitive impairment or poor insight must not drive. If the patient is unable to inform the DVL A, 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 histor y of seizures, the l icense can be reconsidered 6 months after surger y if seizure-free.

● Pituitar y Tumor (Craniotomy): 6 months off driving ; for trans-sphenoidal surger y, driving may resume when there is no residual impairment l ikely 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):

● DVL A must be informed. A PK1 form (appl ication for driving l icense holders' state of health) should be completed.

MCQ TIPS

● Epilepsy vs. Syncope:

○ Key Point: Syncope often involves brief loss of consciousness with quick recover y, whereas epilepsy involves postictal confusion and prolonged recover y

○ 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 decits.

○ 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 decits.

● 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 abil ity through regular assessments.

● Multiple Sclerosis (MS):

○ Key Point: MS patients may continue to drive if their condition is stable, but they must inform the DVL A if they experience signicant symptoms affecting their driving abil ity.

○ 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 l icense.

● Driving Post-Seizure: After a rst seizure, patients must be seizure-free for 6 months before reapplying to the DVL A.

● Stroke and TIA: For most cases, patients can resume driving after 1 month if they have recovered satisfactorily and have no residual decits.

● Dementia: Continuous monitoring and regular assessments are crucial Patients with advanced dementia should not drive, and healthcare professionals must inform the DVL A if the patient cannot .

Note:

At MedRevisions, we have dedicated years to helping candidates excel in the PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

Normal Pressure Hydrocephalus (NPH)

Over view

Normal Pressure Hydrocephalus (NPH) is a potentially reversible condition characterised by the classic triad of:

1 Gait disturbance (magnetic gait)

2 Urinar y 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 signicant increase in intracranial pressure

CAUSES

NPH can be categorised as:

1 . Idiopathic (Primar y) NPH:

○ Most common type

○ Cause of CSF buildup is unknown

○ Linked to age-related changes in CSF absorption

2. Secondar y NPH:

○ Caused by an identiable underlying condition that obstructs CSF ow or absorption:

■ Head trauma

■ Subarachnoid hemorrhage

■ Meningitis

■ Brain tumor

■ Prior brain surger y

■ Idiopathic intracranial hyper tension

EPIDEMIOLOGY

● Prevalence: More common in individuals over 60 years of age.

● Gender: Sl ight male predominance.

● Risk Factors: Age, histor y of head trauma, subarachnoid haemorrhage, meningitis, or other conditions affecting CSF dynamics.

CLINICAL FEATURES

● Gait Disturbance:

○ Often, the earl iest symptom is described as a "magnetic gait , " where the feet seem stuck to the oor.

● Urinar y Incontinence:

○ Star ts as urgency or frequency and may progress to over t incontinence.

● Cognitive Decl ine:

○ Memor y 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 signicant cor tical atrophy. Enlarged lateral and third ventricles are typical, with a relatively preser ved cor tical mantle.

○ Classic Finding :

■ Ventriculomegaly with an absence of signicant cor tical 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

Alzheimer ’s Disease

Parkinson’s Disease

More prominent early memor y loss, language difficulties, and visuospatial decits than NPH. MRI typically shows cor tical atrophy, par ticularly in the temporal lobes.

If the question describes a patient with signicant memor y loss and language difficulties in the early stages, along with cor tical atrophy on imaging, think AD.

Vascular

Dementia (VaD)

Resting tremors, bradykinesia, rigidity, and postural instabil ity are hallmark features. Cognitive impairment and urinar y incontinence are later manifestations of PD

Look for the classic motor symptoms of PD and the absence of early prominent cognitive or urinar y symptoms

Stepwise decl ine in cognitive function, often with focal neurological decits (e g , weakness, sensor y changes) corresponding to areas of stroke or ischemic injur y. Imaging shows multiple lacunar infarcts or white matter changes.

Other Dementias

Consider frontotemporal dementia (FTD) if behavioural changes and personal ity are more prominent than memor y loss Lewy body dementia (LBD) can cause visual hallucinations, uctuations in cognition, and parkinsonism.

A histor y of vascular risk factors (hyper tension, diabetes, smoking ) and a stepwise decl ine with focal neurological signs should raise suspicion for VaD.

Be aware of the unique features of different dementias and the corresponding imaging ndings.

Medication Side

Effects Review the patient's medication l ist for drugs that can cause gait

If the question mentions a recent medication change or

disturbances, urinar y incontinence, or cognitive impairment (e.g., antichol inergics and benzodiazepines).

polypharmacy, consider drug -induced causes in the differential.

Subdural

Hematoma Often, a histor y of head trauma, even minor. Symptoms can uctuate, with headache, drowsiness, confusion, and focal neurological signs Imaging shows a crescent-shaped collection of blood.

Inquire about recent falls or head injuries, especially in elderly patients with uctuating neurological symptoms and imaging ndings consistent with SDH

Creutzfeldt- Jakob Disease: Rapidly progressive dementia with myoclonus and specic EEG changes.

KEY POINTS FOR PL AB 1

● Symptoms: Triad of gait disturbance, urinar y incontinence, and cognitive decl ine is key to diagnosing NPH.

● Imaging : Ventriculomegaly without signicant cor tical atrophy on MRI or CT

● Management: Ventriculoperitoneal (VP) shunting can signicantly improve symptoms, especially gait disturbances

MANAGEMENT

● Initial Management:

○ Symptomatic treatment addressing gait instabil ity, cognitive decl ine, and urinar y incontinence as needed.

● Denitive Treatment:

○ Ventriculoperitoneal (VP) Shunting: The mainstay of treatment , often leading to improvement in gait and, to a lesser extent , cognitive and urinar y symptoms.

● Follow-Up:

○ Regular monitoring post-shunt placement for compl ications l ike shunt malfunction or infection.

COMMON CONFUSIONS FOR PL AB 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 preser ved cor tical 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 PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

Cauda Equina Syndrome (CES)

Over view

Cauda equina syndrome (CES) is a rare but severe condition caused by compression of the cauda equina, a bundle of ner ve 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, urinar y 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 signicant gender predilection

Risk Factors

● Lumbar Disc Herniation: Most common cause, par ticularly large central herniations.

● Spinal Stenosis: Narrowing of the spinal canal that compresses the cauda equina.

● Trauma: Ver tebral fractures or dislocations.

● Tumors: Spinal metastases or primar y spinal tumors.

● Infections: Epidural abscesses or osteomyel itis.

● Postoperative Compl ications: Especially after lumbar spine surger y.

● Inammator y Conditions: Ankylosing spondyl itis

Pathophysiology

Cauda equina syndrome occurs when there is signicant compression of the ner ve roots at the cauda equina level, leading to impaired motor and sensor y function in the lower l imbs and bladder/bowel dysfunction. Compression may result from:

● Herniated disc

● Spinal stenosis

● Tumors

● Trauma

● Other space-occupying lesions

Cl inical 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 sensor y loss in the perineal region, including the inner thighs and area around the buttocks.

● Bladder and Bowel Dysfunction: This may present as urinar y retention, incontinence, or loss of bowel control

Additional symptoms may include:

● Lower Limb Weakness: Motor weakness in the lower extremities, often affecting gait and mobil ity.

● Sexual Dysfunction: Loss of sexual function due to ner ve involvement .

Differential Diagnosis

Lumbar Disc Herniation Unilateral leg pain, no saddle anaesthesia or bowel/bladder dysfunction.

Multiple Sclerosis Bowel/bladder symptoms with additional neurological signs (e.g., optic neuritis).

Spinal Cord Compression

Peripheral Neuropathy

Conus Medullaris Syndrome

Investigation

Involves upper motor neuron signs due to involvement above the cauda equina.

Common in diabetes, usually lacks acute severe pain or urinar y symptoms.

Similar to CES but with more prominent upper motor neuron signs and early bladder dysfunction.

● Cl inical Examination: Assess for lower l imb weakness, saddle anaesthesia, and diminished reexes.

● 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 urinar y retention if cl inical suspicion exists, but should not delay imaging.

Management

Stage Inter vention

Immediate Surgical Decompression

Steroid Use

Preoperative Analgesia

Bladder Care

Postoperative Physiotherapy

Details

The mainstay of treatment is typically within 48 hours of symptom onset

Cor ticosteroids may reduce inammation but are not a substitute for surger y

Adequate pain control, often with opioids.

Catheterisation may be necessar y to rel ieve urinar y retention.

Rehabil itation to improve mobil ity and strength.

Bladder and Bowel Training For those with residual dysfunction.

Psychological Suppor t

Prognosis

Address the emotional impact of the condition and its compl ications.

● Timing of Surger y: Critical in determining outcomes. Delays can lead to permanent neurological decits.

● Residual Symptoms: Despite timely surger y, some patients may experience ongoing bladder, bowel, or sexual dysfunction.

● Rehabil itation: 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 denitive investigation. X-rays are not sensitive for CES, and CT is less commonly used unless MRI is contraindicated.

● Management Priorit y: Immediate surgical consultation is crucial. Watch out for distractors in MCQs that suggest non-surgical inter ventions l ike physiotherapy or delayed imaging.

● Confounding Symptoms: Be cautious when differentiating CES from other causes of radicular pain or neurological decits, such as MS or spinal cord compression, by focusing on the presence of perineal sensor y loss and bowel/bladder symptoms

● Understanding the Red Flags: Students must be aware of "red ag" symptoms such as saddle anaesthesia, urinar y retention, and acute onset of bilateral lower l imb weakness, which necessitate urgent referral and management .

KEY POINTS FOR PL AB 1

● Surgical Emergency: CES is an urgent condition requiring immediate surgical decompression.

● Red Flags: Bilateral sciatica, saddle anesthesia, and urinar y retention are critical signs.

● Urgent MRI: The investigation of choice to conrm the diagnosis.

● Early Inter vention: Vital for preventing permanent neurological damage.

Note:

At MedRevisions, we have dedicated years to helping candidates excel in the PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

Restless Leg Syndrome (RLS)

Over view

Restless Leg Syndrome (RLS), also known as Will is-Ekbom Disease, is a neurological disorder characterised by an irresistible urge to move the legs, often accompanied by uncomfor table sensations These symptoms primarily occur during periods of rest or inactivity, par ticularly in the evening or at night , and are temporarily rel ieved by movement . The exact aetiology of RLS is not fully understood, but it is bel ieved to involve the dopaminergic pathways in the brain. RLS is often chronic and can signicantly impact sleep and qual ity of l ife.

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

Cl inical Features

Symptoms

Uncontrollable urge to move the legs (Akathisia)

Symptoms predominantly occur at night

Symptoms worsen with rest

Paraesthesias

Details

The primar y symptom of RLS, often described as a need to rel ieve an uncomfor table sensation.

Initially affecting night-time, symptoms may progress to daytime as the condition worsens

The discomfor t typically intensies when the patient is lying down or sitting for extended periods.

Patients often describe these sensations as "crawl ing," "throbbing," or "itching "

Periodic Limb Movements of Sleep (PLMS)

Temporar y rel ief of symptoms with movement

Causes and Associations

Involuntar y, repetitive movements of the legs during sleep can disturb both the patient and their bed par tner.

Symptoms are temporarily rel ieved by activities l ike walking or stretching

Cause/Association Details

Genetic predisposition Positive family histor y is noted in around 50% of idiopathic cases.

Iron deciency anaemia RLS is often associated with low iron levels, and correcting the deciency can improve symptoms

Pregnancy Par ticularly in the third trimester, symptoms are common and typically resolve postpar tum.

Uraemia Often seen in patients with chronic kidney disease

Diabetes mell itus Peripheral neuropathy associated with diabetes can increase the risk of RLS.

Diagnosis

● Cl inical Diagnosis: Based on the histor y of symptoms, especially the pattern of symptom rel ief with movement and exacerbation at rest .

● Laborator y Tests: Blood tests are useful to exclude iron deciency anaemia, with serum ferritin levels <50 ng/mL indicating a potential need for iron supplementation.

Differential Diagnosis and MCQ Tips

Condition

Key Differentiators

Peripheral Neuropathy Can present with similar sensor y disturbances but typically lacks the characteristic urge to move the legs. Often associated with diabetes or vitamin deciencies

Spinal Cord Tumors May present with similar sensor y symptoms and discomfor t , but often with associated motor decits or back pain.

Infections (e.g., Spinal Epidural Abscess)

Nocturnal Leg Cramps

Iron Deciency

Presents with back pain, fever, and neurological decits; this is a medical emergency

These are painful, often involve calf muscles, and are not associated with an urge to move the legs.

Even in the absence of anaemia, low ferritin levels (<50 ng/mL) can contribute to RLS symptoms Consider checking and correcting iron levels.

MCQ Tips:

● First-Line Treatment: Dopamine agonists such as Ropinirole or Pramipexole are the rst-l ine treatment for RLS. Gabapentin and pregabal in are also used, par ticularly in patients with painful RLS or those with contraindications to dopamine agonists.

● Iron Supplementation: Indicated if ferritin levels are below 50 ng/mL, as low iron levels are associated with RLS.

● Avoidance of Worsening Factors: Caffeine, nicotine, and cer tain medications (e g , antihistamines, antidepressants) can exacerbate RLS symptoms.

● Pregnancy: RLS is common in pregnancy, and symptoms often resolve postpar tum Non-pharmacological measures are preferred, but iron supplementation is safe if needed.

Management

Pharmacological Management:

1 . Dopamine Agonists:

○ Pramipexole and Ropinirole are the rst-l ine treatments for moderate to severe RLS. They are par ticularly effective in reducing symptoms but may have side effects l ike nausea and dizziness

2 Gabapentin/Pregabal in:

○ Effective for patients with painful RLS or those who do not respond to dopamine agonists or have contraindications Also useful in patients with coexisting neuropathic pain.

3. Iron Supplementation:

○ If ferritin levels are low (<50 ng/mL) , consider oral or intravenous iron supplementation.

4. Benzodiazepines:

○ Clonazepam may be used, especially if insomnia is a signicant problem, but it is not rst-l ine due to dependency risks.

5. Avoid Antipsychotics:

○ Antipsychotics l ike haloperidol should generally be avoided, as they can exacerbate RLS symptoms.

Non-Pharmacological Management:

● Sleep Hygiene: Encourage good sleep habits, as RLS symptoms are often worse with poor sleep

● Exercise: Regular, moderate exercise can help alleviate symptoms but avoid excessive exercise, which may worsen symptoms

● Avoidance of Aggravating Factors: Caffeine, nicotine, and alcohol can worsen RLS symptoms.

Common Confusions for PL AB 1

1 . Differentiating from Peripheral Neuropathy:

○ Remember that the key feature of RLS is the urge to move the legs, which is not typically seen in neuropathy.

2 Role of Iron Supplementation:

○ Only indicated if ferritin levels are below 50 ng/mL.

3. First-Line Treatment:

○ Dopamine agonists are the go-to treatment , not antipsychotics or typical neuropathic pain medications l ike carbamazepine.

Note:

At MedRevisions, we have dedicated years to helping candidates excel in the PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more

Guillain-B arré Syndrome (GBS)

Over view

Guillain-Barré Syndrome (GBS) is an acute, immune-mediated polyneuropathy that primarily affects the peripheral ner vous system. It is characterised by rapidly progressing symmetrical weakness and areexia, often with sensor y disturbances. The syndrome is often triggered by a preceding infection, par ticularly gastrointestinal or respirator y infections, and is associated with molecular mimicr y, where the immune system attacks the peripheral ner ves mistakenly.

Epidemiology

Aspect Details

Incidence GBS is relatively rare, affecting 1-2 individuals per 100,000 annually.

Age Can occur at any age but is more common in adults, par ticularly males

Preceding Infections

Pathogenesis

About 75% of GBS cases are preceded by an infection, with Campylobacter jejuni being the most common pathogen associated with GBS.

● Cross-reaction of antibodies with gangl iosides in the peripheral ner vous system.

● Anti-GM1 antibodies are found in approximately 25% of GBS patients.

Fact Highl ight: Anti-GQ1 b antibodies are present in 90% of Miller Fisher Syndrome (MFS) cases, a variant of GBS presenting with ophthalmoplegia, areexia, and ataxia.

Cl inical Features

Feature

Details

Weakness Star ts distally in the lower l imbs and ascends symmetrically. Progresses over hours to days, with peak severity usually reached within 2-4 weeks. May progress to involve respirator y muscles, necessitating mechanical ventilation. Facial weakness and bulbar involvement (dysphagia, dysar thria) are common.

Reexes

Sensor y Symptoms

Autonomic Dysfunction

Areexia or hyporeexia is a hallmark of GBS. Deep tendon reexes are diminished or absent early in the disease.

Mild sensor y loss, par ticularly paraesthesia, typically in a glove-and-stocking distribution Pain, especially radicular pain in the back and l imbs

Fluctuations in hear t rate, blood pressure instabil ity, and bladder dysfunction. Severe autonomic dysfunction is a poor prognostic indicator.

Differential Diagnosis and MCQ Tips

Condition

Multiple Sclerosis (MS)

Myasthenia Gravis

Key Differentiators

Episodes of neurological decits with recover y, typically involving optic neuritis, sensor y loss, and upper motor neuron signs l ike spasticity and hyperreexia.

Differentiation: Multiple sclerosis often presents with upper motor neuron signs (e.g., hyperreexia, spasticity) and has a relapsing -remitting course GBS, on the other hand, is a lower motor neuron disorder with hyporeexia or areexia and does not exhibit the characteristic central ner vous system lesions seen on MRI in MS

Fatigable muscle weakness, ptosis, and diplopia Typically involves cranial muscles early, and reexes are usually preser ved.

Differentiation: Myasthenia gravis involves fatigable weakness, par ticularly affecting the ocular and bulbar muscles rst Unl ike GBS, reexes remain intact , and there is no ascending paralysis.

Polymyositis

Botul ism

Tick Paralysis

Descending symmetrical paralysis star ts with cranial ner ve involvement , autonomic dysfunction, and respirator y muscle involvement .

Differentiation: Botul ism causes descending paralysis, star ting with cranial ner ves and progressing downwards, which is the opposite of the ascending paralysis seen in GBS.

Descending paralysis, star ting with cranial ner ves Reexes are typically preser ved

Rapidly progressive ascending paralysis without sensor y changes, resolving after tick removal.

Transverse Myel itis

Chronic Inammator y Demyel inating Polyneuropathy (CIDP)

Differentiation: Tick paralysis mimics GBS but resolves rapidly after the tick is removed. The absence of autonomic symptoms and normal CSF ndings distinguish it from GBS.

Motor and sensor y decits below the level of the spinal cord lesion, often with a sensor y level and sphincter dysfunction

Chronic, progressive or relapsing course, symmetric weakness, and sensor y loss with elevated CSF protein.

Differentiation: CIDP presents with a more chronic, progressive course compared to the acute onset of GBS. Patients may have relapsing episodes over months to years, unl ike the typically monophasic course of GBS

Peripheral Neuropathy

Gradual onset of sensor y and motor symptoms, often star ting distally and progressing proximally. Common causes include diabetes and chronic alcohol abuse.

Differentiation: Unl ike GBS, peripheral neuropathies typically have a chronic and insidious onset , with symptoms progressing slowly over months to years. Reexes might be diminished, but the progression is not as rapid as in GBS.

Spinal Cord Tumors

Infections (e.g., Spinal Epidural Abscess)

Asymmetrical weakness, sensor y loss, and back pain. May have signs of spinal cord compression, such as hyperreexia below the level of the lesion.

Differentiation: Spinal cord tumours often present with local ised back pain and asymmetrical motor or sensor y symptoms. MRI is crucial for diagnosis and will show a mass lesion compressing the spinal cord, which is absent in GBS.

Acute onset of back pain, fever, and neurological decits Can progress to severe back pain with radicular symptoms and spinal cord compression.

Differentiation: Infections l ike spinal epidural abscess are typically associated with systemic signs of infection (e g , fever) and acute back pain, often preceding neurological symptoms. GBS lacks fever and usually presents with more symmetrical ascending paralysis.

MCQ Tips:

● Preceding Infection: A histor y of recent gastrointestinal or respirator y infection, par ticularly with Campylobacter jejuni, should prompt consideration of GBS.

● Pattern of Weakness: Ascending symmetric weakness star ting from the lower extremities and progressing upwards is typical of GBS. Reexes are usually absent or diminished.

● CSF Analysis: Elevated protein levels with a normal cell count ("albuminocytologic dissociation") is a hallmark of GBS.

● Respirator y Involvement: Look for signs of respirator y muscle weakness, which can necessitate ICU admission and mechanical ventilation.

● Ner ve Conduction Studies: These are crucial for diagnosis, showing reduced conduction velocities and possible conduction block in GBS.

● Autonomic Dysfunction: GBS can cause autonomic instabil ity, leading to uctuating blood pressure, arrhythmias, and abnormal sweating.

Investigations

Investigation Details

Ner ve Conduction Studies (NCS)

Lumbar Puncture

Spirometr y

Blood Tests

First-Line Investigation: Conrms demyel ination with reduced conduction velocities, conduction block, and prolonged distal latencies.

Early NCS may be normal; repeat studies are recommended if initial results are inconclusive

Cerebrospinal Fluid (CSF): Typically shows elevated protein levels without pleocytosis (albuminocytologic dissociation) , which may develop 1-2 weeks after symptom onset .

Forced Vital Capacity (FVC): Essential for monitoring respirator y function and determining the need for ICU admission

Include FBC, LFTs, electrolytes, and serology to rule out other causes and assess for compl ications.

Elevated hepatic aminotransferases may indicate severe disease

Electrocardiogram (ECG) Necessar y to monitor for arrhythmias due to autonomic involvement .

Management

First-Line Treatment:

1 . Intravenous Immunoglobul in (IVIG):

○ Typically administered over 5 days

2. Plasma Exchange (Plasmapheresis):

○ Another rst-l ine therapy, par ticularly effective if star ted early in the disease course.

Suppor tive Care:

● Monitoring: Intensive monitoring for respirator y failure and autonomic instabil ity.

● Respirator y Suppor t: Mechanical ventilation may be necessar y in severe cases.

● Thromboprophylaxis: Due to immobil ity and risk of thromboembol ism.

● Pain Management: Neuropathic pain may require analgesics l ike gabapentin or carbamazepine.

Rehabil itation:

● Early initiation of physiotherapy and occupational therapy to prevent compl ications and promote recover y.

Prognosis

● Recover y usually begins 2-4 weeks after the plateau of disease, but the timel ine can var y.

● Most patients achieve signicant recover y, though up to 20% may have residual weakness

● Relapses are rare, but vigilance for recurrence is necessar y.

Key Points for MCQs:

● Preceding Infection: A histor y of recent gastrointestinal or respirator y infection, par ticularly with Campylobacter jejuni, should prompt consideration of GBS.

● Pattern of Weakness: Ascending symmetric weakness star ting from the lower extremities and progressing upwards is typical of GBS. Reexes are usually absent or diminished.

● CSF Analysis: Elevated protein levels with a normal cell count ("albuminocytologic dissociation") is a hallmark of GBS.

● Respirator y Involvement: Look for signs of respirator y muscle weakness, which can necessitate ICU admission and mechanical ventilation.

● Ner ve Conduction Studies: These are crucial for diagnosis, showing reduced conduction velocities and possible conduction block in GBS.

● Autonomic Dysfunction: GBS can cause autonomic instabil ity, leading to uctuating blood pressure, arrhythmias, and abnormal sweating.

Note:

At MedRevisions, we have dedicated years to helping candidates excel in the PL AB 1 exam, and we’re now applying our decade-long exper tise to the UKML A. With the PL AB exam now al igned with the ML A 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 cl inical scenarios, and that comes with experience.

To suppor t your learning, we’ve l inked exam-style questions directly to our notes for immediate reinforcement . Plus, our Study Essential Mode helps you efficiently cover the entire ML A content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your cl inical 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 PL AB 1 Candidates say about MedRevisions

● Was MedRevisions enough to pass the August 2024 PL AB exam (exam based on the ML A content map): Find out what this doctor ’s experience was

● 5000+ UKML A and PL AB 1 Exam style questions

● Unl imited timed mocks

● Spaced repetition learning tool

● And much more