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LMNL vs. UMNL

LMNL vs. UMNL. Dayna Ryan, PT, DPT Winter 2012. General terminology. PNS: motor units and associated sensory connections Includes cranial nerves CNS: brain and spinal cord Sign = an objective finding revealed upon physical examination

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LMNL vs. UMNL

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  1. LMNL vs. UMNL Dayna Ryan, PT, DPT Winter 2012

  2. General terminology • PNS: motor units and associated sensory connections • Includes cranial nerves • CNS: brain and spinal cord • Sign = an objective finding revealed upon physical examination • Symptom = (subjective) functional components of a disease perceived by a patient and expressed in a patient’s history

  3. Peripheral nerve conditions • Bell’s Palsy • Guillain-Barre • Charcot-Marie-Tooth Disease • Polio and post-polio syndrome • Diabetic polyneuropathy • Alcoholic polyneuropathy • Hansen’s Disease (leprosy) • Mixed peripheral nerve / spinal cord conditions • Myotrophic lateral sclerosis (ALS) • Tabesdorsalis

  4. Lower Motor Neuron Lesions • Most common signs/symptoms: pain and weakness • Muscle weakness • Paralysis (plegia) = total or severe loss of voluntary contraction • Paresis = mild or partial loss of voluntary contractioncharacteristic of LMNLs • Atrophy – common feature of many neuromuscular disorders • -if you don’t use it u lose it. • Hypertrophy • Compensatory activation of synergistic muscles to support weakened muscles may result in “compensatory hypertrophy) • Causes muscle imbalance, and can lead to pain.

  5. Muscle hyperactivity • Fasciculations = rapid, fine, painless contraction of groups of muscle fibers • Visible but not strong enough to move limbs • Commonly seen in anterior horn cell disorders=motor cells (e.g. ALS) • Cramps = painful muscle spasms • When violent, referred to as convulsions • Clonic: alternating contraction and relaxation • Tonic: sustained contraction=charley horses • Also associated with anterior horn cell disorders

  6. Tetany • = involuntary muscle twitching, spams, or cramps occurring as a result of a hyperexcitable peripheral nerve • **can also occur in CNS disorders • Fibrillation: small, asynchronous contractions occurring in a single skeletal muscle fiber • Too small to see (need an EMG to detect) • Present following denervation and with some myopathies • Myotonia: delayed capacity for relaxation in skeletal muscle (tone disorder) • Contracture: tightness or restricted ROM across a joint (common for Parkinson's, due to basal ganglia)

  7. LMNL Characteristics • Muscle Fatigability (myasthenia) • Decreased muscle endurance because cannot recruit because of lack of innervation • Hypotonia: decreased muscle tone • Increased risk of subluxation (shoulders, scoliosis) • Abnormal Sensation • Often an early presenting sign of PNS dysfunction • Paresthesias = tingling or “pins and needles” sensations • Decreased or absent DTRs • Due to disrupted reflex arc (motor or sensory path) • Myopathies exhibit this because muscle cannot respond to the nerve impulse

  8. Sensory Abnormalities that Accompany LMNLs • Anesthesia: Loss of feeling or sensation, especially the loss of pain. • Hypesthesia: Decreased sensitivity to sensory stimulation; also called hypoesthesia. • Paresthesia: Abnormal sensation such as burning, pricking, tickling, or tingling, especially occurring spontaneously. • Hyperesthesia: Exaggerated unpleasant sensitivity to touch or other non-noxious sensory stimuli.

  9. Sensory Abnormalities that Accompany LMNLs • Hypalgia: Diminished sensitivity to painful stimuli:; also called hypoalgia. • Hyperalgia: Excessive sensitivity to painful stimuli. • Causalgia: sensation of persistent, severe burning of the skin, often accompanied by hypersensitivity to touch and temperature and trophic skin changes

  10. *EXAM*: Upper Motor Neuron Lesions • Spasticity = velocity-dependent increased muscle tone accompanied by hyperactive DTRs • Any damage to the corticospinal tract causes spasticity (crosses at medulla pyramids) • Predominantly in anti-gravity muscles (UE flexors, LE extensors) • Caused by lack of inhibition to control excitability of alpha motor neurons • Rigidity = increased resistance to passive stretch that is velocity independent and uniform throughout ROM • -much harder to stretch than spasticity • Occurs in basal ganglia and extrapyramidal disorders • Cogwheel: rhythmic, interrupted resistance (Parkinson’s=only really sever) • Decorticate: usually from lesions in the thalamus, cerebral white matter, or internal capsule • Decerebrate: from lesions in midbrain or diencephalon

  11. Rigidity from Brain Injury Fredericks & Saladin book “Pathophysiology of the Motor Systems”

  12. Upper Motor Neuron Lesions • Hypotonia: associated with cerebral or spinal shock, followed by an increase in spasticity • Muscle Weakness/Generalized Fatigue • significant atrophy is rare since reflex activity is still present • Poor Coordination • Loss of fractionation • Movement timing: increased reaction time & increased movement time (time to build up contraction and complete movement) • Involuntary movements (tremors, choreas, athetosis, etc)

  13. Upper Motor Neuron Lesions • Associated reactions = unintentional movement of one limb that often occurs during the intentional movement of another limb • Ataxia = unsteadiness, incoordination, or clumsiness of movement • Movement is jerky and unprecise • Difficulty regulating force, direction, and velocity of movement • Common in cerebellar lesions • Apraxia = inability to perform a goal-directed motor activity in the absence of paresis, ataxia, or disturbance of muscle tone • Sensory deficits – larger areas compared to PNS lesions

  14. Brain Stem

  15. Brainstem Lesions

  16. Brainstem Lesions

  17. Bell’s Palsy • Innervation to upper face is bilateral • Innervation to lower face is unilateral (from opposite hemisphere) • “a” is Bell’s Palsy • “b” is stroke • Person in a and b requested to smile and close eyes

  18. Bell’s Palsy: Etiology • Unknown in most cases • May be secondary to viral infection causing swelling in auditory canal or exposure to cold temperatures • In a small number of cases, secondary to acoustic neuroma impinging on nerve

  19. Bell’s Palsy: Signs & Symptoms • Motor: flaccidity • Mouth droops • Nasolabial fold is flattened • Eyelid does not close • Sensory: • Decreased taste on ipsilateral tongue • ANS: • Decreased tearing (dry eye) Characteristic Smile

  20. Bell’s Palsy: Incidence and Onset • Incidence is 20/100,000 in US each year (affects 20,000-100,000 people in US / year) • Typical onset is overnight • Onset more common between 20-40 y.o. (increased incidence with increased age) • Increased risk in diabetics and pregnant women and people with MS

  21. Bell’s Palsy: Medical Treatment • High-dose corticosteroids for 5 days followed by a tapered dose for another 5 days • Antiviral medications, e.g. acyclovir • Because of positive association between HSV and Bell’s Palsy • Improves outcomes when paired with corticosteroids • Eye patch, artificial tears (methylcellulose eye drops every 4 hours) • Gentle massage and gentle heat occasionally used • PT for muscle retraining only if problems persist

  22. Diabetic Polyneuropathy • Affects PNS axons primarily (some demyelination) • Etiology: disrupted microcirculation • Onset: • After long duration diabetes • In diabetics who have had diabetes for 25+ years, 50% have this condition • Occurs in insulin-dependent and non-insulin dependent diabetes • Some regeneration with control of diabetes

  23. Diabetic Polyneuropathy • Characteristics • Large nerve fiber involvement (most common) • painlessparesthesias in feet and lower legs • decreased vibration and proprioception sense • decreased DTRs • Small nerve fiber involvement • deep aching pain in legs and burning feeling in feet • decreased touch, pain, and temperature sensations • nocturnal pain and paresthesias

  24. Diabetic Polyneuropathy • Screening/Examination Tests • NCVs • Monofilament screening with 5.07 / 10 gm. filament • Vibration • Complications • Diabetic ulcers (reducing WB helps) • 50% of non-traumatic amputation in US are in diabetic patients

  25. Alcoholic Polyneuropathy • Affects PNS axon and myelin • Characteristics • Distal muscle weakness and atrophy • Sensory involvement greater in LEs than in UEs • Pain and paresthesias in distal legs and soles of feet (this does not typically happen in the diabetic polyneuropathy) • Aching in calf muscles • Decreased ankle reflexes and poor sensation in feet

  26. Alcoholic Polyneuropathy • Cause • Insidious onset and slow progression • Exacerbations may occur • Sensory signs and symptoms before motor • Mild case = mild aching in calf and feet • Severe case = severe motor and sensory signs • Prognosis • with abstinence and improved nutrition, a slow, incomplete recovery may occur • considerable discomfort may remain

  27. Stocking-Glove Pattern of Sensory Impairment

  28. Charcot-Marie-Tooth (CMT) Disease • Also known as: • Hereditary Motor and Sensory Neuropathy Type I (HMSN) OR • Peroneal Muscular Atrophy • Lesion site = PNS axon and PNS demyelination, anterior horn cell and dorsal root ganglion • Onset • Hereditary • Late childhood or adolescence for CMT1 • Adulthood for CMT2 (less severe with minimal sensory loss) • Slowly progressive

  29. Charcot-Marie-Tooth (CMT) Disease • Characteristics • Pescavus foot deformity (high arch) and hammer toes • Symmetric weakness and atrophy in intrinsic foot, peroneal, and anterior tibialis muscles • Weakness and atrophy rarely go above knee or elbow • Paresthesias are common • Lead to foot drop (see steppage gait pattern) • Normal lifespan – most remain ambulatory throughout their lives

  30. Charcot-Marie-Tooth Disease • Foot deformity: high arch pescavus foot deformity with hammer toes

  31. Tabes Dorsalis • Lesion site: dorsal roots & posterior columns of lumbosacral and lower thoracic S.C. • Etiology: From syphilis • Diagnosis based on: • Neuroimaging is normal • Abnormal tibial sensory NCVs • CSF has elevated protein level • Significant sensory loss!

  32. TabesDorsalis • Characteristics • Unilateral or bilateral presentation • Diminished proprioception and vibration in legs • Sensory ataxia of gait • Areflexia • Touch, pain, and temperature sensation are intact • Aching / paresthesias (radicular distribution) • May also have: • Autonomic disturbances (bladder atony(incontinence), papillary abnormalities, impotence) • Later onset of distal muscle weakness and atrophy (if anterior horn cells become involved)

  33. Hansen’s Disease (Leprosy) • Lesion site: Peripheral nerves • Etiology: Mycobacterium leprae infection • Two forms: • Tuberculoid • Primarily superficial nn • Leprous • Weakness - symmetric • Sensory loss • Skin lesions

  34. Guillain-Barre Syndrome (GBS) • Alternate Name: Acute Inflammatory DemyelinatingPolyradiculoneuropathy = AIDP • Many variants of the syndrome exist • Lesion site • PNS myelin (secondary axonal degeneration in many patients) • Etiology • autoimmune disorder with unknown trigger (may be secondary to an upper respiratory or GI infection)

  35. Guillain-Barre Syndrome (GBS) • Primary Characteristics • Weakness • typically symmetric, beginning in distal LE muscles and ascending through body rapidly including facial muscles • facial and palatal weakness is common ( in about 50% of cases) • Paresthesias (usually transient) • Diminished or absent DTRs • Flaccid muscle tone

  36. Guillain-Barre Syndrome (GBS) • Early symptoms • difficulty with walking • paresthesia in toes (commonly 1st symptom) • muscle tenderness (tender to touch) • About 50% have respiratory involvement • up to 30% of GBS patients require mechanical ventilation during the acute phase • Dysarthria=slurring of words, dysphagia=difficulty swallowing, and diplopia=double vision develop in severe cases

  37. Guillain-Barre Syndrome (GBS) • Can occur at any age, but mostly 5th-8th decade • Disease course: • Maximal onset in less than 4 weeks, many in a few days • Static phase (plateau of 2-4 weeks) • Recovery takes months to years • Recurs in 10% of cases Static Phase Recovery Onset Weeks

  38. Guillain-Barre Syndrome (GBS) • 5% mortality rate • At 6 months, 85% are ambulatory • At 1 year, 20% remain significantly handicapped by weakness • At 2 years, 8% have not achieved full recovery • Poorer prognosis with: • onset at an older age • protracted time before recovery begins • need for artificial respiration • significantly decreased amplitude of evoked motor potential (a sign of axonal degeneration)

  39. Polio & Post-Polio Syndrome (PPS) • Also called: Post-Polio Muscular Atrophy (PPMA) • Lesion site: anterior horn cells (little CN involvement) • Etiology • Polio virus initially. • Existing motor neurons reduce the number of collateral sprouts resulting in more muscle cell death. • As motor neurons die with age, there is no redundancy in the system for other motor units to take over, so motor function is decreased. • NOT due to reactivation of the polio virus.

  40. Polio & Post-Polio Syndrome (PPS) • Decades after onset of polio (mean of 25 years post-polio onset) • ¼ to ½ of polio survivors are expected to develop post-polio syndrome (some sources say up to 2/3 of all polio survivors will get PPS) • more common in women than men • occurs more frequently in those with more severe initial polio symptoms

  41. Polio & Post-Polio Syndrome (PPS) Signs and Symptoms • Sensation • Not affected • Joint and muscle pain • Intolerance to cold •  Motor • Paresis or flaccid paralysis • Decreased or absent DTRs=lmn • Decreased endurance for physical activity Exercise recommendations: • Never exercise to point of fatigue (use general body conditioning and low resistance exercises) • Monitor vitals before and after exercise (remember that respiratory muscles are also affected) • Caution patient to stop exercise if pain persists or weakness increases

  42. Polio & Post-Polio Syndrome (PPS) • Original signs & symptoms • Asymmetric paralysis • Leg affected more than arm • More severe proximally than distally • No eye muscles involved (CN involvement usually only temporary) • Post-polio S & S • Decreased strength in previously affected muscles • New muscle weakness • Increased muscle atrophy • Myalgia • Joint pain

  43. Amyotrophic Lateral Sclerosis (ALS) • Also called Lou Gehrig’s Disease • Lesion site: anterior horn cells, lateral corticospinal tract, motor nuclei of brainstem, and motor area of frontal lobe (pre-central cortex) • Etiology unknown except in a few inherited cases

  44. Amyotrophic Lateral Sclerosis (ALS) • LMN signs • Progressive muscle wasting • Weakness (asymmetric weakness is often presenting sign) • Fasciculations (especially evident in tongue) • cramps • UMN signs • Spasticity • Hyperreflexia • Positive Babinski

  45. Amyotrophic Lateral Sclerosis (ALS) • Most common to see: • Weakness (greater in UEs than in LEs) • Atrophy • Fasciculations • Increased DTRs • Positive Babinski • Later may see dysphagia and dysarthria • Onset: • 90% of all cases have onset between 40-70 years of age • Course is variable and progressive to all striated muscles (except extraocular) • Death typically secondary to respiratory muscle involvement

  46. Amyotrophic Lateral Sclerosis (ALS) • Prognosis • Death in 2-5 years commonly from respiratory compromise (mean death is 3-4 years after onset if patient does not get ventilatory support) • 20% survive more than 5 years • those who have ALS before age 50 generally live longer

  47. Amyotrophic Lateral Sclerosis (ALS) • Functions typically preserved throughout disease: • Intellect is not affected • Eye movements • Bowel and bladder control • Exercise recommended to: • prevent disuse atrophy • maximize strength in remaining innervated muscle cells • Common problems with swallowing, speech, postural control, and respiration • Treat pain with modalities such as TENS • Scapulohumeral joints may be affected with increased muscle weakness . . . Can get glenohumeral joint subluxation

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