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approachtomuscleweakness modified- By Sir Ghani.pptx
- 1. APPROACH TO WEAKNESS By:- Dr Abdul Ghani Rahimoon 1
- 2. 2 Introduction: • Weakness as professional/ medical term refer to symptom arise from something wrong in muscle. • In this situation very important to differentiate between weakness & other confusing symptoms which mimic weakness as said by patient, as fatigue. • Weakness as mentioned before indicate the wrong is in the muscle, either due to pathology with in muscle (myopathy), or pathology in its motor nervous supply. So power of muscle will be decreased according to MRC power rating system. This we name it, objective muscle weakness, neuromuscular weakness, true muscle weakness or clinical muscle weakness (i.e: clinically detectable muscle weakness).
- 3. • Fatigue is subjective term reported by patient as weakness-like complain felt after exercise but actually muscle power is normal, i.e: no pathology in muscle or in its nerve supply. So fatigue is non- objective muscle weakness, non-neuromuscular weakness, functional muscle weakness or false muscle weakness. Motor Nerve Supply 3 True Muscle Weakness Wrong neither in muscle nor in its nerve supply Function al Muscle weaknes s [Myopathy ] Muscl e
- 4. 4 Why approach to weakness is very important? • Because stroke enter in differential diagnosis of weakness which severe condition & current stroke management mandates urgent evaluation of unilateral limb weakness.
- 5. 5 Classification by Algorithm-wise Approach: First of all keep in your mind the following helping questions: • Mode of Onset & Duration: oAcute: vascular, toxic & metabolic. oChronic: neoplastic, infective, inflammatory, endocrine, degenerative diseases. • Course: oWorse at onset then get regress later on: neurogenic cause: vascular. oProgressive: neurogenic cause: neoplasm, degenerative & infective diseases. oEpisodic: neurogenic cause: vascular. oActivity dependent: NMJ cause: MG & muscular cause: myopathies.
- 6. 6 o UMNL or LMNL signs.
- 7. 7 Reviews: Stroke: •Most common cause of unilateral weakness. •Patients typically present with sudden onset of the complains. •If persist < 3 hours , then it will resolve (TIA), while if persist > 3 hours, then it will not resolve (true stroke). •It can be cortical ,subcortical, brainstem or spinal
- 8. •How to approach stroke. 1. Identify nature whether ischemic or hoemorrhagic. If ischaemic then embolic or thrombotic.We have to ask three question,1. time of stroke, 2.deficit at onset and 3.progression. Thrombotic stroke usually occurs at 4 am, while embolic and heomorrhagic usually during activity. Embolic give rise to fixed deficit but deficit progresses in thromotic.
- 9. LOCALIZATION 2. Site/localization. Before localization try to understand some words The words are. 1. Hemilegia vs hemiparesis 2. Dense hemiplegia,brachial (upper limb more weaker than lower limb) and crural (lower limb more weaker than upper limb) hemiplegia. 3.crossed (cranial nerve manifestation on one side and hemiplegia on other side) and uncrossed hemiplegia (both cranial nerve manifestation and hemiplegia on same side)
- 11. All cranial nerves has dual/bilateral supply from hemispheres except some part of facial and some part of hypoglossus
- 12. • Now how to say that stroke is cortical, The hemiplegia will be either crural or brachial and there may be cortical dysfunction as mentioned below 1 2
- 13. -How to say internal capsule. Answer is dense hemiplegia. No cortical sign. -Qustion, which site is more common for thrombotic, cortical or internal capsule? -How to say subcortical stroke??
- 14. Space-occupying lesions (SOL): e.g. tumors, abscesses, chronic subdural hematoma, can cause symptoms & signs mimicking stroke but the onset is typically more gradual & progressive. •There may be features of raised ICP. 10
- 16. Other midbrain syndromes Perinaud. Claude Nothnagel benedict
- 17. Pontine syndrome
- 19. Pseudobulbar vs bulbar palsy
- 20. can spinal cord lesion manifest as hemiplegia Yes, if hemicut above c5
- 21. 11 Spinal cord lesions: •Above level of C5: oHemicut: Ibsilateral UMN hemiparesis/ hemiplegia and deep hemiparesthesia with contralateral superficial hemiparesthesia. oComplete cut: UMN quadriparesis/ quadriplegia with bilateral loss all sensation types. N.B: If injury involve C3, C4 & C5, then patients will be died (because these are root values of phrenic nerve). •C5 to T1 (brachial plexus): oHemicut: ibsilateral LMN hemiparesis/ hemiplegia and deep hemiparesthesia with contralateral superficial hemiparesthesia in upper limbs & ibsilateral UMN hemiparesis/ hemiplegia and deep hemiparesthesia with contralateral superficial hemiparesthesia in lower limbs.
- 22. 12 o Complete Cut: bilateral LMN weakness with bilateral loss of all sensation types in upper limbs & bilateral UMN weakness with bilateral loss of all sensation types in lower limbs. •T2 to L1: oHemicut (Brown Sequard syndrome): ibsilateral UMN or LMN monoparesis/ monoplegia in lower limb with ibsilateral deep sensory loss & contralateral sensory loss take sensory level pattern on trunk & autonomic dysfunction symptoms. oComplete cut: UMN (spastic) paraparesis/ paraplegia or LMN (flaccid) paraparesis/ paraplegia with or without sensory loss take sensory level pattern on trunk & autonomic dysfunction symptoms.
- 23. 13
- 24. 14 •Below L1 (Lumbosacral Plexus/ Cauda-Equina): always LMN weakness in lower limbs unilaterally or bilaterally but not to similar extent with sensory loss take “glove & stocking” pattern & autonomic dysfunction symptoms.
- 25. By the way: 15
- 26. Multiple Sclerosis (MS): 16 •Idiopathic inflammatory demyelinating disease of white matter of the brain and spinal cord. •Common in women between 20 – 40 years. •Usually monosymptomatic. •Characterized by relapsing & remitting course. •Presented with motor, ocular sensory, cerebellar, autonomic or cranial nerves abnormalities. The ocular abnormality is the most common one. •Can presented with almost any pattern of UMN limb weakness, though paraparesis secondary to TM is the most typical.
- 27. AHC Lesions; Motor Neuron Diseases (MND): 17 •It’s group of chronic degenerative diseases of unknown etiology affecting the motor system only. •Characterized by gradual onset and progressive weakness. •Common in males > 50 years. •Affect UMN or LMN or both. Can be presented with bulbar symptoms. •No sensory, cerebellar, autonomic or ocular abnormalities.
- 28. Peripheral nerve lesions: • Cause LMN limbs weakness. • Can be caused by: o Metabolic causes: DM, Renal failure, Hypoglycemia. o Inflammatory causes: GBS, Sarcoidosis, Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP). o Toxins: Botulism, Lead, Alcohol. o Vasculitis: RA, PAN, Wegener’s granulomatosis. o Drugs: INH, Phenytoin, Cisplatin. o Congenital: Charcot Marie Tooth disease. 18
- 29. Guillain-barre Syndrome: 19 •It is acute ascending inflammatory demyelinating polyneuropathy that is autoimmune in nature. •Can affect any age. • Presentation is acute. • H/O URTI, diarrhea, vaccination 2 weeks before the presentation. • Symmetrical ascending weakness of regressive course. • Dyspnea is alarming sign.
- 30. 20 NMJ lesions; Myasthenia Gravis (MG): •Autoimmune neuromuscular disorder characterized by fatigable LMN muscle weakness. •Common in women between 20 – 40 years. •Type of weakness is fatigable & of diurnal variation, i.e: muscle power initially is normal then get weakens with repeated activity to became true weakness at end of day. •Associated with ocular & bulbar symptoms & tend to be affected before limb muscles. •Occur as relapsing & remitting course
- 31. Muscle Lesions; Myapathies (Proximal LMN weakness): 21 • Inflammatory Myopathy: polymyositis, dermatomyositis, vasculitis. • Infectious Myopathy: o Bacterial: pyomyositis, Lyme myositis. o Viral: influenza, parainfluenza, Coxsackie, HIV, CMV, echovirus, adenovirus, EBV. o Fungal infections. o Parasitic: trichinosis, toxoplasmosis. • Drug/Toxic Myopathy: steroid, alcohol, cocaine, heroin, colchicine, antimalarial, statins, fibrates, penicillamine, zidovudine, gemcitabine. • Endocrine Myopathy: hypothyroidism, hyperthyroidism, Cushing’s, diabetes, acromegaly. • Metabolic Myopathy: hypokalemia, hypocalcemia, hypophosphatemia, hyponatremia, hypernatremia, disorders of carbohydrate/ lipid/ purine metabolism. • Neoplastic Myopathy: paraneoplastic syndrome. • Rhabdomyolysis: o Drugs: alcohol, cocaine, statins, neuroleptic malignant syndrome, malignant hyperthermia. o Hyperactivity: seizures, exertion. o Trauma/ Operation.
- 32. Remember that: 22 •Muscle Power: preserved in patients with cachexia despite advanced generalized muscle atrophy. In contrast, patients with true muscle weakness due to myopathy have low muscle power generally have normal muscle bulk at time of presentation. •Muscle Tenderness: usually not associated with one of the causes of true muscle weakness, except for infectious myopathies, certain drug- induced myopathies, rhabdomyolysis, thyroid myopathy, and inherited metabolic myopathies.
- 33. Diagnosis By Algorithm- wise Approach: Patient complain of weakness Is the weakness, true? Is the true weakness is strictly unilateral? Unilateral weakness Do blood sugar test This mean cortical stroke excluded by far extent & lesion is in spinal cord (paraparesis/ paraplegia) Is the onset, sudden? Is it associated with features of acute limb ischemia (pain, cold, pale, mottled skin & absent pulse)? Request vascular surgeon consultation Urgent Spine MRI • Cord compression • Intrinsic spinal cord pathology (Syringomyelia, TM, glioma, abscess) Immobilize patient & do cervical spine image if there is h/o trauma Severe back pain + sparing of proprioception & vibration? Request neurosurgeon or oncologist consultation Spinal infarction Are there UMN signs? Is it associated with sensory level & sphincter disturbance? Is there MRI evidence of myelopathy? • Cord compression • Intrinsic spinal cord pathology (Syringomyelia, TM, glioma, abscess) • SCDD (plasma vitamin B12) • Post- radiotherapy myelopathy (Hx) • MND; ALS (Hx & Ex) Bilateral intracranial lesions: cerebral emboli/ metz, venous stroke, demyelination/ MS (Hx & Ex and brain image) This is mean LMN signs Are there sensory s/s? Peripheral neuropathy (distal weakness): GBS (Hx, Ex, NCS, LP, vital capacity monitor) Refer to neurologist CIDP (Hx, Ex, NCS, FBS, HIV test, urinary porphyrin, serum protein electrophoresis) Refer to neurologist Bilateral radiculopathy (Hx, Ex, spinal cord image) Refer to neurologist Otherwise: • Ask about drugs/ alcohol Hx, family Hx of charcot’s disease, social Hx of lead exposure …etc • Request following Ix: FBC, BS, U,E&C, ESR, CRP, Ca, RF, TFT Is there muscle fatigability (fatigable/ post-exercise weakness)? Tendon reflexes? MG (Hx, Ex, tensilon test, EMG, anti- Ach receptor AB, thoracic CT) LEMS (anti- voltage- gated calcium channels AB, EMG, screen underlying malignancy) Proximal weakness ? Myopathies Hx: bedridden patient, drugs/ alcohol hx, past medical hx, past surgical hx, h/o trauma …etc Ix: FBC, U,E&C, ESR, CRP, BS, Ca, RF, TFT, CK, EMG • Infective myopathy (FBC, ESR, PCT) • Some drugs induced myopathy (statin) • Myositis; polymyositis, dermatomyositis (anti-synthetase AB) • Insist on considering peripheral neuropathy, MND, mononeuritis multiplex, myopathies, generalized weakness secondary to acute illness, functional weakness. • Refer to neurologist if no cause identified. Ye s Functional weakness (fatigue) No Ye s Ye s No Ye s No Ye s Ye s No Ye s No Ye s No Ye s No No No Ye s Absen t Normal Ye s No No Is there weight Loss? Is there pallor? Anemia s MG Drugs/ alcohol Hx? • Alcohol • Cocaine abuse • Chronic aspirin ingestion • Anxiety • Depression • Fibromyalgia • Aldosteronism Is there fever? • TB • SBE • Collagen diseases • Other infections Neurologic findings? Is there Polyuria? • Hyperthyroidism • DM • DI • Hyperparathyroidism • CKD • Electrical disturbances • Neoplasm • Malnutrition • Addison’s disease • Cirrhosis • Malabsorption syndrome • CHF • Parkinson’s disease • Muscular dystrophy • MND (ALS) • MS • Neuropathies No Yes No Ye s Is the fatigue constant? Yes No +ve -ve Ye s No -ve +ve No Ye s Is the onset, sudden? Is it painful ? Ischemia (compare pulse & capillary refilling between 2 limbs) Refer to vascular surgeon Fracture (Hx of trauma & do X- ray) Refer to orthopedist Compartment syndrome (CK level in blood) Stroke TIA Are there seizure, evidence of increased ICP, cortical dysfunction or CNS infection? • SOL • Meningoencephaliti s (fever, purpuric skin rashes & meningeal irritation signs) • LP • Neuroimage Are there UMN signs? Is there contralateral sensory loss? Unilateral spinal cord lesions MRI Spine • Ipsilateral sensory loss: SOL, stroke, MS • Normal sensation: MND Is signs are referable to single nerve root/ single nerve? Radiculopathy or mononeuropathy • Insist on considering plexopathy, multi-root compression, MND, stroke, migraine, functional weakness. • Refer to neurologist if no cause identified. Ye s Ye s Is duration > 3 hours? Yes No No Ye s No Ye s Ye s No No No Ye s MRI Spine Ye s No Muscle Tenderness No Other myopathies Ye s No MotorCortex Spinal Cord Peripheral Nerves NM J Muscle Bilateral True Weakness Unilateral True Weakness Functional Weakness 23
- 34. cases
- 35. Sources: 24 • Macleod's Clinical Diagnosis 2nd Ed (2013) • Approach to Internal Medicine 4th Ed (2015) • Algorithmic Diagnosis of Symptoms and Signs 4th Ed (2017) • Toronto Notes 34th Ed (2018) • Ain-Shams University Internal Medicine curriculum (2014) • Decision Making in Medicine 3rd Ed (2010)
- 36. THANK YOU 25