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PNS disorders Nursing.pptx

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The document discusses disorders of the peripheral nervous system (PNS). It defines the PNS and describes its components. Common symptoms of PNS disorders include weakness, numbness and pain localized to parts of limbs. Signs include lower motor neuron signs like atrophy and fasciculations. Select major PNS disorders are then discussed in more detail, including anterior horn cell disorders like ALS, nerve root disorders like radiculopathy, plexopathies, mononeuropathies, peripheral neuropathies, myasthenia gravis, trigeminal neuralgia and Bell's palsy. For each, manifestations, diagnostic tests and treatment approaches are summarized.

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PNS Disorders Dr BALAJI B S ASSOCIATE CONSULTANT NEUROLOGY
01-09-2020 2
01-09-2020 3
01-09-2020 4
What is the Peripheral Nervous System? CNS is confined to brain and spinal cord PNS includes (in anatomical order) Anterior horn cell (located within spinal cord) Spinal nerve roots (radicles) Plexi (brachial and lumbosacral) Named peripheral nerves (e.g. median, peroneal) Tiny nerve endings (sensory fibers and tiny branches of lower motor axons at the neuromuscular junction) Neuromuscular junction 5
Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Anterior horn cells (LMN) The PNS (Emphasizing Motor Structures)
Symptoms of PNS Disease Single focal lesions: weakness/numbness/ pain in one limb, often defined to one part of the limb Multiple or diffuse lesions: weakness/ numbness/pain in more than one limb, usually bilateral and distal 7
Signs of PNS Disease Lower motor neuron signs (atrophy, fasciculations) Hyporeflexia or areflexia Patch of sensory loss, or stocking-glove sensory loss Not UMN signs (spasticity, hyperreflexia, upgoing toe) or brain signs (impaired consciousness, cognition, or language) 8
Reflexes repeated Hyperreflexia and spasticity occur with upper motor neuron lesions (CNS) Hyporeflexia, fasciculations, atrophy with lower motor neuron lesions (PNS) 9
Workup Serologies, especially for treatable causes EMG helps localize and characterize lesions of PNS Imaging for some focal lesions, or to exclude CNS mimics (such as cord lesion or stroke) CSF analysis in demyelinating neuropathies, or polyradiculopathy Nerve biopsy 10
Anterior Horn Cell 11
Amyotrophic lateral sclerosis Anterior horn cells (lower motor neurons) and upper motor neurons degenerate Mix of UMN and LMN signs/symptoms Weakness, spasticity, multifocal muscle atrophy No sensory loss from ALS! Loss of speech, swallow, respiration Death in 2-5 years 12
Manifestations Initial: spastic, weak muscles with increased DTRs; muscle flaccidity, paresis, paralysis, atrophy; clients note muscle weakness and fasciculations; muscles weaken, atrophy; client complains of progressive fatigue; usually involves hands, shoulders, upper arms, and then legs Atrophy of tongue and facial muscles result in dysphagia and dysarthria; emotional lability and loss of control occur 50% of clients die within 2 5 years of diagnosis, often from respiratory failure or aspiration pneumonia
Diagnostic Test Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms EMG to differentiate neuropathy from myopathy Muscle biopsy shows atrophy and loss of muscle fiber Serum creatine kinase if elevated (non- specific) Pulmonary function tests: to determine
Therapeutic Interventions Muscle Relaxants : Central Riluzole PT/ OT/ ST Pain Control Tube Feedings Prevention of Infection
Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Radiculopathy
Spinal Nerve Root Disorders Most common: monoradiculopathy (cervical or lumbosacral) Radiating pain, +/- weakness, +/- sensory loss. Reduced reflex for that root level Commonest causes: disk herniation, minor trauma, degenerative change Usually self-limited Image if severe, worsening, or concern for cancer, infection 17
18
G u illa in -B a r r 辿 S y n d r o m e (G B S ) Acute autoimmune inflammatory demyelinating disorder of peripheral nervous system characterized by acute onset of ascending motor paralysis
M a n if e s t a t io n s Most clients have symmetric weakness beginning in lower extremities Ascends body to include upper extremities, torso, and cranial nerves Sensory involvement causes severe pain, paresthesia and numbness Paralysis of intercostals and diaphragmatic muscle Autonomic nervous system involvement: blood pressure fluctuations, cardiac dysrhythmias, paralytic ileus, urinary retention Weakness usually plateaus or starts to improve in the fourth week with slow return of muscle strength
Diagnostic Tests diagnosis made thorough history and clinical examination; there is no specific test CSF analysis: increased protein EMG: decrease nerve conduction Pulmonary function test reflect degree of respiratory involvement
Medical management IVIG OR Plasmapheresis Enteral feeding Tracheostomy
Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Plexopathy
Plexopathy PNS syndrome in one limb not explained by a single spinal root, or by a single named peripheral nerve Causes: trauma or stretch, compression by tumor or hematoma, radiation, diabetic EMG confirms plexopathy Image if compressive lesion suspected 24
Brachial Plexus behind clavicle, in upper thorax 25
Lumbosacral Plexus: Pelvic, Retroperitoneal 26
Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Mononeuropathy
Mononeuropathy Weakness, numbness, pain, paresthesias confined to the distribution of UE: median nerve, radial n., ulnar n. LE: femoral n., sciatic n., peroneal n. Most common causes: entrapment, trauma, prolonged limb immobility (e.g., surgery) 28
Important Mononeuropathies Median mononeuropathy at the wrist (carpal tunnel syndrome) Ulnar mononeuropathy at the elbow (cubital tunnel syndrome) Radial mononeuropathy (Saturday night palsy) wrist and finger drop Peroneal mononeuropathy (e.g., from leg crossing) one cause of footdrop 29
Median n. Ulnar n. Peroneal n. Named peripheral nerves have well-defined sensory territories (and muscle targets) 30
31
Peripheral Neuropathy Distal symmetric polyneuropathy Affects longest sensory/ motor/ autonomic nerves Nerves are dying back Length dependent (stocking glove) Symmetric loss of pain/ temp / vibration/ proprioception; distal reflex loss Usually chronic. Many possible causes! 32
Peripheral polyneuropathy symptoms Initially, feet numb with paresthesia/ pain Symptoms ascend: legs fingertips Distal weakness (feet, or fingers/grip), atrophy, Severe sensory loss can cause steppage gait, sensory ataxia, imbalance, falls Feet prone to injuries, ulcers, deformation (e.g., Charcot foot) Autonomic: orthostasis, bladder and erectile dysfunction 33
Causes of peripheral polyneuropathy Usually toxic or metabolic #1 cause: diabetes & impaired glucose tolerance B12 defeciency Hematologic (e.g., multiple myeloma) or other immunoglobulin disorders (check SPEP) Drugs: Li, chemotherapy Alcoholic neuropathy Liver or kidney disease HIV and neurosyphilis Inflammatory causes: connective tissue disease 34
Workup for peripheral neuropathy? For typical distal symmetric sensory > motor neuropathy: glucose / Hba1c, B12, SPEP Need EMG and more if rapid or severe, prominent weakness, asymmetry, young patient
PNS disorders Nursing.pptx
Manifestations Seen in the muscles that are affected: Ptosis (drooping of eyelids), diplopia (double vision) Weakness in mouth muscles resulting in dysarthria and dysplagia Weak voice, smile appears as snarl Head juts forward Muscles are weak but DTRs are normal Weakness and fatigue exacerbated by stress, fever, overexertion, exposure to
Diagnostic Tests Physical examination and history Tensilon Test: edrophonium chloride (Tensilon) administered and client with myasthenia will show significant improvement lasting 5 minutes SFEMG: senstive Antiacetylcholine receptor antibody serum levels: increased in 80% MG clients; used to follow course of treatment Serum assay of circulating acetylcholine receptor antibodies: if increased, is diagnostic of MG
Therapeutic Interventions Thymectomy- < production of actecycholine antibodies Cholinergic Agents- pyridostigmine, Steroids- predisone Plasmapheresis- remove antibodies from the blood
Trigeminal Neuralgia Pathophysiology Irritation of the trigeminal nerve (5th cranial nerve), affects sensory portion of nerve Etiology Irritation or Chronic Compression Dx: H&P, CT, MRI
Trigeminal Innervation
Signs & Symptoms Intense Pain on One Side of Face Forehead, Cheek, Nose, Jaw Triggered by Touch, Talking, Other Stimulation
Therapeutic Interventions Anticonvulsants Nerve Blocks Surgery to Block Pain Signals
Bells Palsy Pathophysiology/Etiology Inflammation and Edema of Facial Nerve Loss of Motor Control Etiology Unknown Dx: H&P, EMG, rule out stroke
Signs & Symptoms One Sided Facial Pain Weakness Speech Difficulty Drooling Tearing of Eye Inability to Blink
Therapeutic Interventions Prednisone Antiviral Medication Facial physio, facial nerve stimulation Eye drops
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PNS disorders Nursing.pptx

  • 1. PNS Disorders Dr BALAJI B S ASSOCIATE CONSULTANT NEUROLOGY
  • 5. What is the Peripheral Nervous System? CNS is confined to brain and spinal cord PNS includes (in anatomical order) Anterior horn cell (located within spinal cord) Spinal nerve roots (radicles) Plexi (brachial and lumbosacral) Named peripheral nerves (e.g. median, peroneal) Tiny nerve endings (sensory fibers and tiny branches of lower motor axons at the neuromuscular junction) Neuromuscular junction 5
  • 6. Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Anterior horn cells (LMN) The PNS (Emphasizing Motor Structures)
  • 7. Symptoms of PNS Disease Single focal lesions: weakness/numbness/ pain in one limb, often defined to one part of the limb Multiple or diffuse lesions: weakness/ numbness/pain in more than one limb, usually bilateral and distal 7
  • 8. Signs of PNS Disease Lower motor neuron signs (atrophy, fasciculations) Hyporeflexia or areflexia Patch of sensory loss, or stocking-glove sensory loss Not UMN signs (spasticity, hyperreflexia, upgoing toe) or brain signs (impaired consciousness, cognition, or language) 8
  • 9. Reflexes repeated Hyperreflexia and spasticity occur with upper motor neuron lesions (CNS) Hyporeflexia, fasciculations, atrophy with lower motor neuron lesions (PNS) 9
  • 10. Workup Serologies, especially for treatable causes EMG helps localize and characterize lesions of PNS Imaging for some focal lesions, or to exclude CNS mimics (such as cord lesion or stroke) CSF analysis in demyelinating neuropathies, or polyradiculopathy Nerve biopsy 10
  • 12. Amyotrophic lateral sclerosis Anterior horn cells (lower motor neurons) and upper motor neurons degenerate Mix of UMN and LMN signs/symptoms Weakness, spasticity, multifocal muscle atrophy No sensory loss from ALS! Loss of speech, swallow, respiration Death in 2-5 years 12
  • 13. Manifestations Initial: spastic, weak muscles with increased DTRs; muscle flaccidity, paresis, paralysis, atrophy; clients note muscle weakness and fasciculations; muscles weaken, atrophy; client complains of progressive fatigue; usually involves hands, shoulders, upper arms, and then legs Atrophy of tongue and facial muscles result in dysphagia and dysarthria; emotional lability and loss of control occur 50% of clients die within 2 5 years of diagnosis, often from respiratory failure or aspiration pneumonia
  • 14. Diagnostic Test Testing rules out other conditions that may mimic early ALS such as hyperthyroidism, compression of spinal cord, infections, neoplasms EMG to differentiate neuropathy from myopathy Muscle biopsy shows atrophy and loss of muscle fiber Serum creatine kinase if elevated (non- specific) Pulmonary function tests: to determine
  • 15. Therapeutic Interventions Muscle Relaxants : Central Riluzole PT/ OT/ ST Pain Control Tube Feedings Prevention of Infection
  • 16. Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Radiculopathy
  • 17. Spinal Nerve Root Disorders Most common: monoradiculopathy (cervical or lumbosacral) Radiating pain, +/- weakness, +/- sensory loss. Reduced reflex for that root level Commonest causes: disk herniation, minor trauma, degenerative change Usually self-limited Image if severe, worsening, or concern for cancer, infection 17
  • 18. 18
  • 19. G u illa in -B a r r 辿 S y n d r o m e (G B S ) Acute autoimmune inflammatory demyelinating disorder of peripheral nervous system characterized by acute onset of ascending motor paralysis
  • 20. M a n if e s t a t io n s Most clients have symmetric weakness beginning in lower extremities Ascends body to include upper extremities, torso, and cranial nerves Sensory involvement causes severe pain, paresthesia and numbness Paralysis of intercostals and diaphragmatic muscle Autonomic nervous system involvement: blood pressure fluctuations, cardiac dysrhythmias, paralytic ileus, urinary retention Weakness usually plateaus or starts to improve in the fourth week with slow return of muscle strength
  • 21. Diagnostic Tests diagnosis made thorough history and clinical examination; there is no specific test CSF analysis: increased protein EMG: decrease nerve conduction Pulmonary function test reflect degree of respiratory involvement
  • 22. Medical management IVIG OR Plasmapheresis Enteral feeding Tracheostomy
  • 23. Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Plexopathy
  • 24. Plexopathy PNS syndrome in one limb not explained by a single spinal root, or by a single named peripheral nerve Causes: trauma or stretch, compression by tumor or hematoma, radiation, diabetic EMG confirms plexopathy Image if compressive lesion suspected 24
  • 25. Brachial Plexus behind clavicle, in upper thorax 25
  • 27. Neuromuscular junction and muscle Ulnar nerve Brachial plexus C8 spinal nerve root Mononeuropathy
  • 28. Mononeuropathy Weakness, numbness, pain, paresthesias confined to the distribution of UE: median nerve, radial n., ulnar n. LE: femoral n., sciatic n., peroneal n. Most common causes: entrapment, trauma, prolonged limb immobility (e.g., surgery) 28
  • 29. Important Mononeuropathies Median mononeuropathy at the wrist (carpal tunnel syndrome) Ulnar mononeuropathy at the elbow (cubital tunnel syndrome) Radial mononeuropathy (Saturday night palsy) wrist and finger drop Peroneal mononeuropathy (e.g., from leg crossing) one cause of footdrop 29
  • 30. Median n. Ulnar n. Peroneal n. Named peripheral nerves have well-defined sensory territories (and muscle targets) 30
  • 31. 31
  • 32. Peripheral Neuropathy Distal symmetric polyneuropathy Affects longest sensory/ motor/ autonomic nerves Nerves are dying back Length dependent (stocking glove) Symmetric loss of pain/ temp / vibration/ proprioception; distal reflex loss Usually chronic. Many possible causes! 32
  • 33. Peripheral polyneuropathy symptoms Initially, feet numb with paresthesia/ pain Symptoms ascend: legs fingertips Distal weakness (feet, or fingers/grip), atrophy, Severe sensory loss can cause steppage gait, sensory ataxia, imbalance, falls Feet prone to injuries, ulcers, deformation (e.g., Charcot foot) Autonomic: orthostasis, bladder and erectile dysfunction 33
  • 34. Causes of peripheral polyneuropathy Usually toxic or metabolic #1 cause: diabetes & impaired glucose tolerance B12 defeciency Hematologic (e.g., multiple myeloma) or other immunoglobulin disorders (check SPEP) Drugs: Li, chemotherapy Alcoholic neuropathy Liver or kidney disease HIV and neurosyphilis Inflammatory causes: connective tissue disease 34
  • 35. Workup for peripheral neuropathy? For typical distal symmetric sensory > motor neuropathy: glucose / Hba1c, B12, SPEP Need EMG and more if rapid or severe, prominent weakness, asymmetry, young patient
  • 37. Manifestations Seen in the muscles that are affected: Ptosis (drooping of eyelids), diplopia (double vision) Weakness in mouth muscles resulting in dysarthria and dysplagia Weak voice, smile appears as snarl Head juts forward Muscles are weak but DTRs are normal Weakness and fatigue exacerbated by stress, fever, overexertion, exposure to
  • 38. Diagnostic Tests Physical examination and history Tensilon Test: edrophonium chloride (Tensilon) administered and client with myasthenia will show significant improvement lasting 5 minutes SFEMG: senstive Antiacetylcholine receptor antibody serum levels: increased in 80% MG clients; used to follow course of treatment Serum assay of circulating acetylcholine receptor antibodies: if increased, is diagnostic of MG
  • 39. Therapeutic Interventions Thymectomy- < production of actecycholine antibodies Cholinergic Agents- pyridostigmine, Steroids- predisone Plasmapheresis- remove antibodies from the blood
  • 40. Trigeminal Neuralgia Pathophysiology Irritation of the trigeminal nerve (5th cranial nerve), affects sensory portion of nerve Etiology Irritation or Chronic Compression Dx: H&P, CT, MRI
  • 42. Signs & Symptoms Intense Pain on One Side of Face Forehead, Cheek, Nose, Jaw Triggered by Touch, Talking, Other Stimulation
  • 43. Therapeutic Interventions Anticonvulsants Nerve Blocks Surgery to Block Pain Signals
  • 44. Bells Palsy Pathophysiology/Etiology Inflammation and Edema of Facial Nerve Loss of Motor Control Etiology Unknown Dx: H&P, EMG, rule out stroke
  • 45. Signs & Symptoms One Sided Facial Pain Weakness Speech Difficulty Drooling Tearing of Eye Inability to Blink
  • 46. Therapeutic Interventions Prednisone Antiviral Medication Facial physio, facial nerve stimulation Eye drops