Limb Weakness
Summary
Join 5th year medical student Alan Hamda in an enlightening session focused on the complexities of limb weakness. Learn to decode what a patient means when they refer to “weakness” and familiarize yourself with various patterns of weakness. Master the art of history taking, especially when it comes to generating a DDx for limb weakness. Understand the importance of the time course in establishing differentials and discuss various patient cases to connect theory with practical scenarios. Additionally, take part in interactive quizzes to check your understanding and identify areas of improvement. This session also includes content on critical red flags to watch out for, different examination techniques, the implications of limb weakness in stroke patients and various treatment options available. Perfect for all medical professionals interested in gaining a deeper understanding of this common yet puzzling presentation.
Learning objectives
- Understand the general approach to assessing a patient presenting with limb weakness including an understanding of initial management, history taking, narrowing down differentials and examination considerations.
- Learn to identify certain patterns of weakness and appreciate the key information necessary for generating a differential diagnosis for limb weakness including the importance of time course in nervous system diseases.
- Develop an understanding of the common causes of and risk factors for different types of strokes in order to be better prepared to diagnose and manage patients presenting with limb weakness.
- Learn to recognise and understand the significance of red flags in patients presenting with limb weakness and comprehend the areas of examination that could indicate more serious underlying conditions.
- Improve skills in applying learned knowledge to cases by studying real patient cases, making a diagnosis, and preparing a management plan based on the case features and the patient's symptoms and history.
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Alan Hamda (5th Year, Churchill) Limb WeaknessCONTENT 1. Approach to limb weakness/differentials? 2. History taking 3. Examination 4. Case 1 5. Quiz 1 6. Case 2 7. Case 3 8. Quiz 2Limb Weakness • A patient present to A&E with limb weakness what are the first steps? • Always remember A+E & resuscitation à stabilise patient • Limb weakness can be a complex presentation to dissect; it is critical to establish what the patient is referring to when they are referring to ”weakness” • sensation or be in too much pain to move the limbld infact have ataxia, reduced • There are various patterns of weakness (e.g. bilateral lower extremity, hemiparesis, isolated unilateral extremity)Differentials • Establishing the time course is a crucial component of narrowing differentials when • Sudden onset (seconds to mins) – trauma, vascular (stroke/TIA/SAH), hemiplegic migraine • Subacute onset (hours to days) – Guillain-Barré syndrome, venous thrombosis, subdural hematoma, spondylosis, transverse myelitis, nutrient deficiencies (B12/Copper) • Chronic onset (weeks to months) – malignancy, motor neuron diseaseHistory Taking History of presenting complaint Past medical history Drug history Don’t forget to Family history ICE! Social historyHPC • History is the most critical aspect of generating a DDx for limb weakness. • Key information to gather: • Which limb/limbs (establish pattern of weakness), when did it first start, any other symptoms (e.g. sensory/visual/dysphasia/dysarhria), how have triggers), any previous episodes, any limb jerking/loss of continence, recent trauma, any difficulty balancing/coordinating, any changes to speech, any pain • Systems review • Collateral history can be valuablePMH • •troHypertension, Diabetes Mellitus, Hypercholesterolemia, Atrial fibrillation, Endocarditis • Conditions increasing risk of cerebral aneurysms (CTDs, PKD) • Surgical procedures (spinal/brain/vascular – e.g. carotid endarterectomy) • Malignancy • Recent infection/vaccination (e.g. gastroenteritis --> GBS) • Seizures • Head/spinal injury • Meningitis/EncephalitisDHx • Hypercoagulability: COCP, oral HRT, anticoagulants, antihypertensives, statins • Muscular weakness: amiodarone, antithyroid, chemotherapeutics, NSAIDs, statinsSHx • General social context (accommodation/support network/independence) • Smoking • Alcohol (can cause Vitamin B deficiencies) • Recreational drug use (NO and SACD) • Occupation • Travel • Driving FHx • Cardiovascular/Cerebrovascular Disease • Hypertension, Diabetes Mellitus, Hypercholesterolemia • Autoimmune disorders • Malignancy • Hereditary neurological disease (Huntington’s, Alzheimer’s, MND & some forms of epilepsy) • Muscular dystrophy • NeuropathiesRED FLAGS • Preceding trauma • Previously fit and well • Fever, weight loss, night sweats • Reduced GCS • Headache, early morning nausea/vomiting • Loss of bowel/bladder continence, saddle anaesthesia • Visual changesEXAMINATION • General observations/inspection (clues towards autoimmune features) • Full neurological examination (cranial nerves, upper limb, lower limb) • Cardiovascular examination (why?)EXAMINATION • UMN vs LMN, mixed – think MND/SACD • NMJ/Muscle pathology typically cause proximal weakness and doesn’t affect tone/reflexes • “Pyramidal pattern” – extensors disproportionately weaker than flexors in upper limb, vice versa in lower limb • Language deficits (Broca’s/Wernicke’s), Attention deficits (parietal lobe), Eye signs, Sensory symptoms across modalitiesCASE 1Remember neurology ddx = localization x time course Where can we localize this to? Underlying cause?Stroke • Ischaemic (85%) • Rarer causes: sudden drop in BP, venous sinus • Thrombotic thrombosis & carotid artery dissection • Embolic • A transient ischaemic attack or TIA is an episode of neurological dysfunction due to focal brain/spinal • Haemorrhagic (15%) cord/retinal ischaemia without acute infarction • Intracerebral • Subarachnoid • TIA definition shifted from time-based to tissue- basedCauses/risk factors • Ischaemic: age, hypertension, smoking hyperlipidaemia, diabetes mellitus, atrial fibrillation • Haemorrhagic: age, hypertension, arteriovenous malformation, anticoagulation therapy, connective tissue disorders (Marfan’s/EDS/ADPKD)Symptoms and signs • Motor weakness • Cerebral hemisphere: contralateral hemiplegia, contralateral sensory loss, • Speech problems homonymous hemianopia, dysphasia • Swallowing problems • Lacunar: pure motor, sensory, mixed • Visual field defects or ataxia • Brainstem: numerous presentations! • Balance problemsInvestigations • Obs: Blood pressure • Bloods: FBC, Glucose, Clotting “Hyperdense MCA sign” • Non-contrast CT Head – need to exclude Focal hyper-attenuation of haemorrhage prior to thrombolytic therapy + the middle cerebral artery helps rule out other differentials e.g. space- (MCA) due to intraluminal occupying lesion thromboembolic material - • ECG infarction (within 90 mins). • If stroke is confirmed: Carotid Doppler ultrasonography, EchocardiogramTreatment • Aspirin 300mg orally/rectally (as soon as haemorrhagic stroke excluded) • Maintain blood glucose, hydration and oxygen saturation within normal limits • Thrombolysis with alteplase if: • it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial) • haemorrhage has been definitively excluded (i.e. Imaging has been performed)Treatment • Thrombectomy (clot removal) can be performed by interventional neuroradiologist • Offer thrombectomy ASAP within 6 hours of symptoms onset + IV thrombolysis (if within 4.5 hours) for patients with confirmed occlusion of proximal anterior circulation by CTA/MRA • Offer thrombectomy ASAP to patients last known to be well 6-24 hours previously and with confirmed occlusion of proximal anterior circulation by CTA/MRA or if there is potential to salvage brain tissue as shown by CT perfusion or DWI-MRI demonstrating limited infarct core volume • As above + IV thrombolysis (if within 4.5 hours) for occlusion of proximal posterior circulationTreatment • 3 essential components of secondary prevention: 1. Clopidogrel (or Aspirin + MR dipyridamole if Clopidogrel is CI/not tolerated) 2. Statin 80mg (if cholesterol >3.5 mmol/L) – delay until 48 hours due to risk of haemorrhagic transformation 3. Anti-hypertensivesComplications • Lasting neurological deficit (measured by NIHSS) • Cerebral oedema (malignant MCA syndrome) • Seizures • Amnesia • Increased risk of pneumonia/UTI • Pressure ulcers • Mobility problems/falls • Breathing/swallowing difficulties • Coma • DeathQuestion 1 An 80-year-old man presents to his general practitioner due to an episode of loss of vision and weakness in his left arm this morning. This episode lasted 20 minutes with complete recovery. He is asymptomatic at the time of presentation. He discloses a similar episode occurring two days prior however did not seek medical a diffusion-weighted magnetic resonance imaging scan which shows an area of infarction.o hospital and received A: Hypoglycaemia causing the focal weakness and loss of vision B: Stroke due to the presence of acute infarction on imaging C: Migraine due to the symptoms and the lack of infarction on imaging D: Transient ischaemic attack (TIA) due the lack of infarction on imaging E: Transient ischaemic attack (TIA) due the symptoms lasting < 24 hoursQuestion 1 An 80-year-old man presents to his general practitioner due to an episode of loss of vision and weakness in his left arm this morning. This episode lasted 20 minutes with complete recovery. He is asymptomatic at the time of presentation. He discloses a similar episode occurring two days prior however did not seek medical a diffusion-weighted magnetic resonance imaging scan which shows an area of infarction.o hospital and received A: Hypoglycaemia causing the focal weakness and loss of vision B: Stroke due to the presence of acute infarction on imaging C: Migraine due to the symptoms and the lack of infarction on imaging D: Transient ischaemic attack (TIA) due the lack of infarction on imaging E: Transient ischaemic attack (TIA) due the symptoms lasting < 24 hours Question 2 Department by ambulance with sudden-onset one-ency No other neurological findings. sided weakness and sensory changes. She is triaged as a potential stroke and is quickly reviewed by a What artery was most likely affected? doctor who notes the following examination findings: B: Left anterior inferior cerebellar artery C: Left middle cerebral artery D: Right anterior cerebral artery E: Right middle cerebral artery Question 2 Department by ambulance with sudden-onset one-ency No other neurological findings. sided weakness and sensory changes. She is triaged as a potential stroke and is quickly reviewed by a What artery was most likely affected? doctor who notes the following examination findings: B: Left anterior inferior cerebellar artery C: Left middle cerebral artery D: Right anterior cerebral artery E: Right middle cerebral arteryQuestion 3 A 45-year-old woman presents to her general practitioner with complaints of muscle weakness, predominantly affecting her hips and shoulders. The weakness is more noticeable post-exertion and improves with rest. She reports no pain but experiences some blurring of vision in the evenings, which she attributes to fatigue. On examination, there are no dermatological findings. What is the most likely diagnosis? A: Dermatomyositis B: Lambert-Eaton myasthenic syndrome C: Myasthenia gravis D: Polymyalgia rheumatica E: PolymyositisQuestion 3 A 45-year-old woman presents to her general practitioner with complaints of muscle weakness, predominantly affecting her hips and shoulders. The weakness is more noticeable post-exertion and improves with rest. She reports no pain but experiences some blurring of vision in the evenings, which she attributes to fatigue. On examination, there are no dermatological findings. What is the most likely diagnosis? A: Dermatomyositis B: Lambert-Eaton myasthenic syndrome C: Myasthenia gravis D: Polymyalgia rheumatica E: PolymyositisCASE 2Myasthenia gravis • Autoimmune disease mediated by antibodies to nAChR on post-synaptic side of the neuromuscular junction (Type II hypersensitivity) • Associations • Autoimmune disease: RA, SLE, autoimmune thyroid disorders & pernicious anaemia • Thymoma (15%) • Thymic hyperplasia (50-70%)Symptoms and signs • Presentation: Slowly increasing muscular fatigue which becomes worse with periods of activity and improves with rest. This affects the following muscle groups in order of most common: extraocular, bulbar, face, neck, limb girdle, trunk • Signs: Ptosis, diplopia, eyelid fatiguability (when asked to look up), peek sign (orbicularis oculi fatigue causing eye to involuntarily open as patient tries to keep eyes shut), voice fades on counting to 50, slurred speech, difficulty swallowing, shortness of breathInvestigations • Single fibre electromyography: high sensitivity (92-100%) – decremental muscle response to repetitive nerve stimulation • CT thorax - exclude thymoma • Check creatinine kinase (CK) - exclude dermatomyositis/polymyositis • Antibodies to acetylcholine receptors (anti-nAChR) • positive in around 85-90% of patients • In remaining patients about 40% are positive for anti-muscle-specific tyrosine kinase antibodies (anti-MuSK) • Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used any more due to the risk of cardiac arrhythmia • Ptosis improves by >2mm after application of ice to eyelid for >2 min (why?)Management • Long-acting acetylcholinesterase inhibitors (pyridostigmine) • Immunosuppression • Prednisolone • Azathioprine, cyclosporine, mycophenolate mofetil, rituximab (anti-CD20, depletes B cells) • Thymectomy via video-assisted thoracoscopic surgery (VATS)Complications • Myasthenic crisis: life-threatening weakness of respiratory muscles during a relapse • Monitor FVC regularly • Contact ICU for potential ventilatory support • Plasmapheresis or IV immunoglobulins • Identify + treat underlying trigger for relapse (e.g. infections or medication – tetracyclines, gentamicin)CASE 3A 26-year-old presents to her GP complaining of a weak left leg. She describes that she first noticed an odd tingling sensation spreading up her leg about a week ago, which is still present. A few days after the tingling, she found herself tripping over several times in a single day. By this morning, she was limping and could not manage the stairs at home alone. Nothing like this has ever happened before and she does not recall any trauma. She has never been admitted to hospital before but says that about a year ago she had some eye problems whilst travelling in Africa. She recalls that her right eye became painful and that she had blurred vision for almost a week, before it gradually resolved. She did not seek medical help at the time as she was ‘in the middle of nowhere’ and put it down to ‘some weird infection’. She currently takes the combined oral contraceptive pill and sumatriptan for her occasional migraines. Her family history is unremarkable. She does not smoke and drinks only very occasionally. There are a number of notable features on neurological examination: when you get Mrs Bean to rapidly move her eyes from extreme right gaze to extreme left gaze, you notice that the right eye is slow to adduct relative to the left and abnormal nystagmus of the left eye. Adduction on convergence is normal. In addition, there is a relative afferent pupillary defect (Marcus Gunn pupil) on the right. On examination of her limbs you find that despite the tingling in her left leg, sensation in both legs is objectively intact. However, her left leg has increased tone, decreased power (3/5 on hip flexion and knee flexion), brisk patellar reflex, an upgoing plantar reflex, but normal coordination. Although she has not noticed anything in her right leg, this too has decreased power considering the patient’s young age (4/5 on hip flexion and knee flexion), although tone, reflexes, and coordination are normal on the right.CASE 3 • Time course – 1 week, previous episodes, painful eye + blurred vision (? Optic neuritis) • Bilateral lower extremity weakness + paraesthesia suggests localisation to the spinal cord is likely à bilateral cortical pathology is less common • Episodic attacksMultiple sclerosis • Chronic cell-mediated autoimmune disease characterised by inflammatory plaques (“sclera”) in the CNS disseminated in space and time • Due to a combination of genetic and environmental factors • Female:Male – 3:1, Median age of onset 30, more common at higher latitudes (Vitamin D theory) • Classified based on disease patternSymptoms and signs • Can be non-specific, 75% have significant lethargy • Visual: optic neuritis (presenting feature in 20%), optic atrophy, Uhthoff's phenomenon (worsening of vision following rise in body temperature), internuclear ophthalmoplegia (INO) • Sensory: pins/needles, numbness, trigeminal neuralgia, Lhermitte’s syndrome (paraesthesia in limbs on neck flexion) • Motor: spastic weakness (most commonly in legs) • Cerebellar: ataxia, tremor • Other: urinary incontinence, sexual dysfunction & intellectual deteriorationInvestigations • MRI Brain + Spine MRI shows multiple image demonstrating hyperintense cord multiple • Lumbar puncture - CSF – oligoclonal bands of IgG on lesion some of which periventricular electrophoresis which are not present in serum enhance peripherally demyelinating following gadolinium plaques extending • Visual-evoked potentials (VEPs) administration radially away from the body of the lateral ventricle. These are characteristic of Dawson's fingers in a patient with known multiple sclerosis.Treatment • Aim is to reduce the frequency + duration of relapses • Exercise, stop smoking, avoid stress • Acute relapse: high-dose corticosteroids (methylprednisolone) for 5 days to shorten length of relapse (does not alter degree of recovery) • Disease modifying drugs: • Natalizumab – antagonises alpha-4 beta-1-integrin found on the surface of leucocytes, strongest evidence base for preventing relapse • Ocrelizumab - anti-CD20 • Fingolimod – sphingosine 1-phosphate receptor modulator (prevents lymphocytes exiting lymph nodes) • Beta-interferon • Glatiramer acetate • Manage spasticity – baclofen and gabapentin • Urinary urgency/frequency: if post- micturition residual urine >100mL, teach intermittent self-catheterization; if <100mL, try tolterodine.Question 4 A 35-year-old man presents with progressive weakness of his hands. On examination you notice wasting of the small muscles of the hand. A diagnosis of syringomyelia is suspected. Which one of the following features would most support this diagnosis? A: Hyperreflexia in the upper limbs B: Loss of vibration sensation in the hands C: Loss of temperature sensation in the hands D: Loss of light touch sensation in the hands E: Fasciculation of the small muscles of the hand15% Fasciculation of the small muscles of the handQuestion 4 A 35-year-old man presents with progressive weakness of his hands. On examination you notice wasting of the small muscles of the hand. A diagnosis of syringomyelia is suspected. Which one of the following features would most support this diagnosis? A: Hyperreflexia in the upper limbs B: Loss of vibration sensation in the hands C: Loss of temperature sensation in the hands D: Loss of light touch sensation in the hands E: Fasciculation of the small muscles of the hand15% Fasciculation of the small muscles of the handQuestion 5 A 24-year-old man presents with lower limb weakness. He states that he had an episode of food poisoning two weeks ago which consisted of severe abdominal pain and profuse non-bloody diarrhoea. Following this, he noticed progressive difficulties with balance. His past medical history is largely unremarkable, but he admits to intravenous drug use with heroin. He last injected heroin three weeks ago. On examination, marked ataxia and ophthalmoplegia are noted. What is the most likely diagnosis? A: Acute inflammatory demyelinating polyradiculoneuropathy B: Acute motor axonal neuropathy C: Botulism D: Miller-Fisher syndrome E: TetanusQuestion 5 A 24-year-old man presents with lower limb weakness. He states that he had an episode of food poisoning two weeks ago which consisted of severe abdominal pain and profuse non-bloody diarrhoea. Following this, he noticed progressive difficulties with balance. His past medical history is largely unremarkable, but he admits to intravenous drug use with heroin. He last injected heroin three weeks ago. On examination, marked ataxia and ophthalmoplegia are noted. What is the most likely diagnosis? A: Acute inflammatory demyelinating polyradiculoneuropathy B: Acute motor axonal neuropathy C: Botulism D: Miller-Fisher syndrome E: TetanusQuestion 6 A 62-year-old man is referred to neurology clinic for investigation due to worsening ataxia and paraesthesia in his feet. He gout and hypertension. On examination, there is a loss of joint position and vibration sense. He has brisk knee reflexes andof absent ankle jerks. There is no muscle weakness. What is the most likely diagnosis? A: Chronic inflammatory demyelinating polyneuropathy B: Guillain-Barré syndrome C: Motor neurone disease D: Myasthenia gravis E: Subacute combined degeneration of the cordQuestion 6 A 62-year-old man is referred to neurology clinic for investigation due to worsening ataxia and paraesthesia in his feet. He describes losing his footing very easily and he has had multiple falls in the last few weeks. He has a past medical history of gout and hypertension. On examination, there is a loss of joint position and vibration sense. He has brisk knee reflexes and absent ankle jerks. There is no muscle weakness. • Spinocerebellar à positive What is the most likely diagnosis? Romberg’s sign, sensory ataxia A: Chronic inflammatory demyelinating polyneuropathy (abnormal gait) • Corticospinal à muscle B: Guillain-Barré syndrome weakness, hyperreflexia, brisk C: Motor neurone disease knee reflex, absent ankle jerk, extensor plantars D: Myasthenia gravis • Dorsal column à distal E: Subacute combined degeneration of the cord tingling/burning/sensory loss, impaired proprioception + vibrationSUMMARY 1. What is limb weakness? 2. History taking 3. Examination 4. DDx 1 5. Quiz 1 6. DDx 2 7. DDx 3 8. Quiz 2Please fill out the feedback form Thank you!References 1. https://clinicalproblemsolving.com 2. https://www.passmedicine.com 3. Oxford Cases in Medicine & Surgery 4. Neuroanatomy through Clinical Cases by Blumefield