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APPROACH TO NEUROLOGICAL WEAKNESS.pptx
- 1. APPROACH TO NEUROLOGICAL WEAKNESS Dr.G.VENKATARAMANA MBBS DNB FAMILY MEDICINE
- 2. • Weakness • Reductionin the power that can be exerted by one or more muscles • Fatigability • Inability to sustain the performance of an activity that should be normal for a person of the same age, sex, and size • Bradykinesia • Increased time is required for full power to be exerted • Apraxia • A disorder of planning and initiating a skilled or learned movement unrelated to a significant motor or sensory deficit
- 3. • Paralysis orPlegia Weakness so severe that a muscle cannot be contracted at all • Paresis Less severe weakness • Hemi One-half of the body • Para Both legs • Quadri All four limbs
- 4. • Distribution ofweakness • Weakness from involvement of upper motor neurons occurs particularly in the extensors and abductors of the upper limb and the flexors of the lower limb • Lower motor neuron weakness depends on whether involvement is at the level of the anterior horn cells, nerve root, limb plexus, or peripheral nerve • Myopathic weakness is generally most marked in proximal muscles • Weakness from impaired neuromuscular transmission has no specific pattern of involvement
- 5. • Muscle bulk •Not affected by upper motor neuron lesions,mild disuse atrophy eventually may occur • Atrophy seen in lower motor neuron lesion , Advanced muscle disease • Tone • Resistance of a muscle to passive stretch • Increased in UMN lesions and decreased in LMN lesions • Types • Spasticity • Rigidity • Paratonia • Flaccidity
- 6. • Muscle stretch(tendon) reflexes • Increased with upper motor neuron lesions • Decreased or absent for a variable period immediately after onset of an acute lesion • Hyperreflexia is usually,but not invariably accompanied by loss of cutaneous reflexes (such as superficial abdominals) and, in particular, by an extensor plantar (Babinski) response • The muscle stretch reflexes are depressed with lower motor neuron lesions directly involving specific reflex arcs • Preserved in patients with myopathic weakness except in advanced stages, when they sometimes are attenuated • In disorders of the neuromuscular junction, reflex responses may be affected by preceding voluntary activity of affected muscles • Such activity may lead to enhancement of initially depressed reflexes in Lambert-Eaton myasthenic syndrome and, conversely, to depression of initially normal reflexes in myasthenia gravis
- 7. • Weakness • Reductionin the power that can be exerted by one or more muscles • Grading • Grade 5 Normal power • Grade 4 Movement against resistance • Grade 3 Movement against gravity • Grade 2 Gravity eliminated movement (lateral movements in bed) • Grade 1 There is a visible or palpable flicker of contraction, but no resultant movement of joint • Grade 0 Total paralysis • Grade 4 power covers a broad range – (4 –, 4, and 4+) denoting movement against slight, moderate and stronger resistance
- 8. Where is thelesion? locating the lesion UMN LMN Atrophy - Except disuse atrophy + Fasciculations - + Tone Increased Except when in spinal shock Decreased Distribution of weakness Regional Segmental Muscle stretch reflexes Hyperactive Hypoactive/Absent Superficial reflexes Absent Absent Plantar reflex Extensor (Babinski +) Flexor/Absent
- 9.
- 10. UMN Lesion Features Cortex C/LHemiplegia/Monoplegia C/L 7th CN UMN Seizure/Language/Apraxia Subcortex C/L Hemiplegia/Monoplegia C/L 7th CN UMN Transcortical aphasia Internal capsule C/L Dense Hemiplegia C/L Hemisensory loss C/L 7th CN UMN Homonymous hemianopia Brain stem • Mid brain • Pons • Medulla Crossed hemiplegia Discussed in next slide Spinal cord I/L Hemiplegia I/L loss of Posterior column sensation C/L pain and temperature loss No Cranial nerve involvement
- 11. UMN Brain stem Features Midbrain C/L Hemiplegia C/L 7th CN UMN I/L Opthalmoplegia Pons C/L Hemiplegia I/L 7th CN LMN +/- 6th nerve palsy Medulla - Medial Hemiplegia I/L or C/L or Cruciate I/L LMN 12th cranial nerve palsy MLF – Internuclear opthalmoplegia C/L posterior column sensory loss Medulla- Lateral Crossed sensory (I/L face and C/L body) Horner’s syndrome Ataxia 9th and 10th cranial nerve palsy Hiccups No hemiplegia
- 12. LMN Lesion Features Anteriorhorn cells Asymmetrical Wasting++ > Weakness Distal > Proximal Fasciculations ++ Reflexes variable No sensory/ANS Spinal nerve root/Plexus Asymmetrical weakness Proximal > Distal Reflexes absent Sensory +,Atrophy + Peripheral nerve Symmetrical Weakness +/ - sensory +/-ANS Distal to proximal Reflexes absent Atrophy/Fasciculations+ Neuromuscular junction Generalised Fatiguability/fluctuating (affected by preceding muscle activity) No sensory Muscle Symmetrical Weakness (esp.LL),Proximal > distal No sensory, Reflexes present No wasting( until late) No fasciculations
- 13. What is thelesion? • Etiology • Acute • Vascular • Traumatic • Metabolic • Demyelinating • Subacute • Inflammatory (Demyelinating) • Infection • Neoplasm • Metabolic • Chronic/Insidious onset • Degeneration
- 14. Patterns/Distribution of weakness •Hemiparesis • Paraparesis • Quadriparesis • Monoparesis • Distal weakness • Proximal weakness • Restricted distribution • Ascending vs Descending
- 15. Hemiparesis • Always UMN •Results from an upper motor neuron lesion above the midcervical spinal cord • The presence of other neurologic deficits helps localize the lesion • C/L Cortex / Subcortex / Internal capsule / Brain stem / I/L Upper cervical cord • Acute • Vascular - Stroke • Trauma – Head injury • Todd’s paresis • Sub acute • Infection- Meningoencephalitis,Brain abscess • Demyelination- MS,ADEM • Tumour,Subdural hematoma
- 16. Hemiparesis • Chronic • Tumour •Vascular malformation • Mill’s hemiplegic variant of MND • Investigation of hemiparesis of acute origin usually starts with a CT scan of the brain and laboratory studies • If the CT is normal, or in subacute or chronic cases of hemiparesis, MRI of the brain and/or cervical spine (including the foramen magnum) is performed, depending on the clinical accompaniments
- 17. Paraparesis • Investigations typicallybegin with spinal MRI, but when upper motor neuron signs are associated with drowsiness, confusion, seizures, or other hemispheric signs, brain MRI should also be performed • Electrophysiologic studies - when clinical findings suggest an underlying neuromuscular disorder UMN type LMN type Acute • Acute hydrocephalus • Ant.cerebral artery/SSS thrombosis • Spinal fracture,Spinal abscess • Spinal hematoma • Acute transverse myelitis • Anterior spinal artery thrombosis Acute • UMN in shock • GBS • Polio • Psoas abscess • hematoma Sub acute –Chronic • Parasagittal meningioma • Hydrocephalus • MND (ALS) • Multiple sclerosis • Friedrich ataxia • Subacute combined degeneration Sub acute –Chronic • CIDP • Infective radiculitis(HIV,CMV,HTLV) • MND • Cauda equina • Tabes dorsalis • Myopathies • Peripheral neuropathies
- 18. Quadriparesis UMN type LMNtype • B/L Brainstem lesion • CV junction anomaly • High cervical cord compression • MS • MND • GBS/CIDP • Polio • Peripheral neuropathies • Myopathy • Myasthenia gravis • Snake bite • OPC poisoning • In obtunded patients, evaluation begins with a CT or MRI scan of the brain • If upper motor neuron signs are present but the patient is alert, the initial test is usually an MRI of the cervical cord • If weakness is lower motor neuron, myopathic, or uncertain in origin, the clinical approach begins with blood studies to determine the level of muscle enzymes and electrolytes and with EMG and nerve conduction studies
- 19. Monoparesis Lower limb Upperlimb UMN • ACA territory stroke • SSS thrombosis • Trauma – Frontal lobe contusion • Infection – Granuloma in frontal lobe UMN Stroke – Superior division of MCA Head injury – Parietal contusion LMN • Lumbosacral plexopathy LMN Trauma – Brachial plexus/injury to multiple cervical roots Investigations UMN signs: Brain CT or MRI LMN signs: EMG,NCS
- 20. Distal weakness • Anteriorhorn cells Asymmetrical Wasting++ > Weakness Distal > Proximal Fasciculations ++ Reflexes variable No sensory/ANS • Peripheral nerve Symmetrical Weakness +/- Sensory +/- ANS Distal to Proximal Reflexes absent Atrophy/Fasciculations+
- 21. Proximal weakness • Root/Plexus •Asymmetrical weakness • Proximal > Distal • Reflexes absent • Sensory + • Atrophy + • Muscle • Symmetrical • Weakness (esp.LL) • Proximal > Distal • No sensory • Reflexes present • No wasting( until late)/No fasciculations
- 22. • Restricted distribution •Neuropathy Entrapment Mononeuritis multiplex • Intermittent weakness • Electrolyte disturbances • Channelopathies • Metabolic disorders of muscles
- 23. • Ascending • GBS •Extra medullary compression • Descending • Botulism • Diptheria • Snake bite • Intramedullary compression • Ells berg phenomenon: Anticlock wise • Compressive myelopathy
- 26. Anterior horn celldisease/MND • Chronic: • UMN+LMN:Amyotrophic lateral sclerosis • Pure LMN :X-linked spinobulbar muscular atrophy(kennedy’s),Adult Tac-Sachs,Spinal muscular atrophy • Pure UMN:Primary lateral sclerosis,Hereditary spastic paraplegia • Acute: • Virus (Polio,Herpes Zoster,Coxsackie)
- 27. Plexopathy • Brachial Plexopathy– Neoplasm, Trauma, Brachial neuritis • Lumbosacral Plexopathy – Neoplasm, Psoas abscess
- 29. Neuromuscular junction disorders •Myasthenia Gravis (Post synaptic)- Autoimmune • Lambert Eaton Myasthenic Syndrome (Pre synaptic) – Paraneoplastic • Snake bite (History, Descending) Cobra - Post synaptic Krait - Pre synaptic • Botulism (Descending) • OPC – Intermediate syndrome