Approch to weakness &paralysis pateint (1).pptx

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1. Approach to a patient with weakness and paralysis Prepared by: Girma Abdissa & Ahimed Moderator : Dr. Suleiman (MD ) August,2024

2. General Objectives To differentiate between the pathophysiology of weakness and paralysis versus fatigue, and to acquire knowledge on investigating, examining, and managing patients presenting with weakness and paralysis.

3. Course Outline Introduction Pathogenesis Of weakness Etiology of Weakness Fatigue Approches to pateints for Weakness &paralysis Investiagtions Managemnt principles References

4. INTRODUCTION DEFINITION WEAKNESS Reduced strength in muscles, where individuals can still attempt to move but find it difficult or insufficient. May be due to various factors, including fatigue, nerve damage, or underlying health conditions, have functional limitations (due to pain or limited joint motion) even though muscle strength is normal.

5. Weakness of specific muscle groups can cause disorders of eye movement, dysarthria, dysphagia, or respiratory weakness It is one of the most common reasons patients present to primary care clinicians.

6. PARALYISIS The complete loss of muscle function in a specific area, resulting from disruption in the motor pathways from the brain to the muscles It can affect any part of the body and signifies a more severe impairment than weakness Common causes include: Stroke : Disruption of blood flow to the brain can lead to hemiplegia. Spinal Cord Injury: ( paraplegia or quadriplegia) Infections: ( polio or Guillain-Barré syndrome).

7. Neuromuscular Disorders: ALS and muscular dystrophy). Genetic Disorders: Conditions like periodic paralysis involve inherited factors.(HypoPP and HyperPP)

8. Pathophysiology of Weakness Voluntary movement is initiated in the cerebral motor cortex, at the posterior aspect of the frontal lobe. The neurons involved (upper motor or corticospinal tract neurons) synapse with neurons in the spinal cord (lower motor neurons). Lower motor neurons transmit impulses to the neuromuscular junction to initiate muscle contraction.

9. Common mechanisms of weakness include dysfunction Upper motor neurons (corticospinal and corticobulbar tract lesions) Lower motor neurons (due to peripheral polyneuropathies or anterior horn cell lesions) Neuromuscular junction Muscle (due to myopathies)

10. The location of certain lesions Upper motor neuron dysfunction disinhibits lower motor neurons, increased muscle tone (spasticity) and increased muscle stretch reflexes (hyperreflexia). An extensor plantar (Babinski) reflex is specific for corticospinal tract dysfunction. Upper motor neuron dysfunction can decrease tone and reflexes motor paralysis is sudden and severe (spinal cord transection, in which tone first decreases, then increases gradually over days to weeks) or if the lesion damages the motor cortex of the precentral gyrus and not nearby motor association areas.

11. Lower motor neuron dysfunction disrupts reflex arcs, causing hyporeflexia and decreased muscle tone (flaccidity) and may cause fasciculations (muscles atrophy) Peripheral polyneuropathies tend to be most noticeable in the longest nerves (weakness is more prominent in the distal limb than the proximal and in legs more than arms) and produce signs of lower motor neuron dysfunction (decreased reflexes and muscle tone).

12. The most common disorder of the neuromuscular junction myasthenia gravis typically causes fluctuating weakness that worsens with activity and lessens with rest. Diffuse muscle dysfunction (myopathies) tends to be most noticeable in the largest muscle groups (proximal muscles).

13. Etiology of Weakness The many causes of muscle weakness are categorized by the location of the lesion ,usually lesions in a given location manifest with similar clinical findings Some disorders have characteristics of lesions in more than one location. (Amyotrophic lateral sclerosis (ALS) &disorders of spinal cord may have findings of both upper and lower motor neuron dysfunction(anterior horn cells, or both).

14. 1. Common causes of focal weakness Stroke (the most common cause of unilateral weakness) Neuropathies, including those that are caused by trauma or entrapment (carpal tunnel syndrome) and that are immune-mediated (Bell palsy) Spinal root entrapment (herniated intervertebral disk) Spinal cord compression (cervical spondylosis, epidural cancer metastasis, trauma) Multiple sclerosis Temporary focal weakness may occur as part of postictal (Todd) paralysis, (TIA)

15. 2. The most common causes of generalized weakness are Deconditioning due to inactivity (disuse atrophy) resulting from illness or frailty( older ages) Generalized muscle wasting (prolonged ICU) - a condition called critical illness myopathy Critical illness polyneuropathy (ICU neuropathy) Common myopathies (alcohol myopathy, hypokalemia, corticosteroid myopathy) Use of paralytic agents in a critical care patient

16. Fatigue Fatigue can prevent maximal effort and muscle performance during strength testing. Many patients report weakness when their problem is fatigue. Common causes of fatigue include Acute severe illness of almost any cause, cancers, chronic infectins HIV infection, hepatitis, endocarditis, mononucleosis, endocrine disorders, renal failure, hepatic failure, heart failure, and anemia.

17. Multiple sclerosis can cause daily fatigue that increases with exposure to heat and humidity. Patients with fibromyalgia, depression, or chronic fatigue syndrome may report weakness or fatigue but have no defined objective abnormalities.

18. Approches to pateints of Weakness &paralysis Should try to distinguish true muscular weakness &paralyis from fatigue then check for findings that help establish the location or mechanism (whether weakness &paralyisis are caused by dysfunction of The brain Spinal cord Plexuses Peripheral nerves Neuromuscular junction , or muscles) and the cause.

19. History History of present illness should begin with open-ended questions, asking patients to describe in detail what they are experiencing as weakness. Then, specific questions can be asked, to do specific tasks, brushing teeth or hair, speaking, swallowing, rising from a chair, climbing stairs, and walking. the onset of weakness (sudden or gradual) and progression (constant, worsening, intermittent) of symptoms.

20. Close questioning is needed to differentiate sudden onset from sudden recognition (walking, tying shoes). Important associated symptoms include sensory changes, double vision, memory loss, difficulty using language, seizures, and headaches. Factors that worsen weakness, such as heat ( suggesting multiple sclerosis) or repetitive use of a muscle (suggesting myasthenia gravis )are noted

21. Review of system Should seek symptoms suggesting possible causes, including the following: Daily fatigue and weakness that increases with heat and humidity: Multiple sclerosis Diurnal variation of fatigue and weakness: Myasthenia gravis Rash: Dermatomyositis, Lyme disease, or syphilis Fever : Chronic infection Muscle pain : Myositis Neck pain : Cervical myelopathy Vomiting or diarrhea : Botulism

22. Shortness of breath : Heart failure, a pulmonary disorder, or anemia Anorexia and weight loss: Cancer or other chronic illness Change in color of urine: Porphyria or a liver or kidney disorder Heat or cold intolerance: Thyroid dysfunction Mood disorder : d epressed mood, poor concentration, anxiety, and loss of interest in usual activities:

23. Past medical history Should identify known disorders that can cause weakness &paralyise or fatigue, including Thyroid, liver, kidney, or adrenal disorders Cancer or risk factors for cancer (paraneoplastic syndrome (Eaton-Lambert syndrome) such as heavy smoking) Osteoarthritis (cervical myelopathy) Infections

24. Clinicians should assess risk factors for possible causes, including those for infection Unprotected sexual intercourse, Blood transfusions, Exposure to tuberculosis) Stroke (hypertension, atrial fibrillation, atherosclerosis). Complete drug history should be reviewed.

25. Family history Should include known hereditary disorders hereditary muscle disorders, channelopathies, metabolic myopathies, hereditary neuropathies and presence of similar symptoms Hereditary motor neuropathies often go unrecognized in families because of variable, incomplete phenotypic expression. Hammr toes, high arches in the feet, and poor performance in sports may indicate an undiagnosed hereditary motor neuropathy.

26. Social history Use of alcohol: Suggesting alcohol myopathy Illicit drug use: Suggesting increased risk of HIV/AIDS, bacterial infections, tuberculosis, or stroke due to cocaine use Occupational or other exposure to toxins (organophosphate insecticides, heavy metals, industrial solvents) Recent travel: Suggesting Lyme disease, tick paralysis, diphtheria, or a parasitic infection Social stressors : Suggesting depression

27. Physical examination A complete neurologic and muscle examination is done to identify localizing or diagnostic findings Cranial nerves Motor function Coordination Gait Sensation Reflexes

28. 1. Cranial nerve examination Inspection of the face for gross asymmetry and ptosis Extraocular movements and facial muscles,Palatal weakness(nasal voice quality). Tongue weakness is suggested by inability to clearly articulate certain consonants ( saying "ta-ta-ta") and slurring of speech (lingual dysarthria). Sternocleidomastoid and trapezius strength is tested by having the patient rotate the head and shrug the shoulders against resistance. The patient is asked to blink repeatedly to see whether blinking fatigues.

29. 2. Motor examination Inspection, assessment of tone, and strength testing. Inspected for kyphoscoliosis (suggesting chronic weakness of paraspinal muscles) and for surgical and traumatic scars. Dystonic posturing (torticollis) may interfere with movement, mimicking weakness. Inspected muscles fasciculations and atrophy; both may begin focally or asymmetrically in amyotrophic lateral sclerosis (ALS). Fasciculations may be most visible in the tongue in patients with advanced ALS. Diffuse atrophy may be most evident in the hands, face, and shoulder girdle.

30. Muscle tone is assessed using passive motion . Tapping a muscle ( hypothenar) may induce fasciculations in neuropathies or a myotonic contraction in myotonic dystrophy. Strength testing Should include muscles that are proximal, distal, extensor, and flexor. Some tests of large, proximal muscles include standing from a sitting position; squatting and rising; and flexing, extending, and turning the head against resistance.

31. Motor strength is often rated on a 0 to 5 scale: 0: No visible muscle contraction 1: Visible muscle contraction with no limb movement 2: Limb movement but not against gravity 3: Movement against gravity but not resistance 4: Weakness against resistance 5: Full strength NB : these numbers seem objective, rating strength between 3 and 5 if symptoms are unilateral, comparison with the unaffected side improves discrimination

32. 3. Coordination testing Finger-to-nose and heel-to-shin maneuvers and toe-heel tandem gait to check for cerebellar dysfunction, which can accompany cerebellar stroke, vermian atrophy (alcohol abuse) Hereditary spinocerebellar ataxias, multiple sclerosis, and the Miller Fisher variant of Guillain-Barré syndrome.

33. 4 . Gait is observetion Ignition failure (temporary freezing in place when starting to walk, followed by festination): Parkinson disease Apraxia , as when feet stick to the floor: Normal pressure hydrocephalus or other frontal lobe disorders Festination : Parkinson disease Limb asymmetry, as when patients drag a leg, have reduced arm swing, or both: Hemispheric stroke Ataxia : Midline cerebellar disease Instability during turns : Parkinsonism

34. 5. Sensation teste Sensory deficits can help localize some lesions causing weakness (sensory level localizes the lesion to a spinal cord segment) or suggest certain specific causes of weakness ( distal sensory loss helps confirm clinical suspicion of Guillain-Barré syndrome). A truncal bandlike tingling and pressure in a dermatomal distribution is a spinal cord sign that occurs with both intrinsic and extrinsic lesions.

35. 6. Reflexes are teste If deep tendon reflexes appear absent, they may be elicited by augmentation with Jendrassik maneuver (trying to pull the hands apart while they are clasped together). Hyporeflexia may be normal throughout life or occur with aging, but findings should be symmetric and augmentation should elicit reflexes that are otherwise absent.

36. The following responses suggest certain disorders or locations of lesions: The classic Babinski reflex (the great toe extends and the other toes fan apart) is highly specific for a corticospinal tract lesion (except in infants, where the reflex is physiologic because the corticospinal tract is immature). A normal jaw jerk and hyperreflexic arms and legs suggest a cervical lesion affecting the corticospinal tract, usually cervical stenosis.

37. Anal tone, anal wink reflex, or both are reduced or absent in spinal cord injury but are preserved in ascending paralysis due to Guillain-Barré syndrome. Abdominal reflexes are absent below the level of spinal cord injury (except in ALS where they are inexplicably preserved). A cremasteric reflex can test the integrity of the upper lumbar cord and roots in males

38. Evaluation also include Testing for back tenderness to percussion (present with vertebral inflammation, some vertebral tumors, and epidural abscess) Straight leg raising (painful with sciatica) Checking for scapular winging (suggesting weakness of the shoulder girdle muscles)

39. If patients have no objective motor weakness The general examination is particularly important; nonneuromuscular disorders should be sought. Signs of respiratory distress. The skin is examined jaundice, pallor, rash, and striae, smooth hairless skin, ascites, and vascular spiders of chronic alcohol use The neck, axillae, and inguinal area should be palpated for adenopathy; any thyromegaly is noted.

40. Moon facies of Cushing syndrome and the parotid enlargement Heart and lungs are auscultated for crackles, wheezes, prolonged expiration, murmurs, and gallops. The abdomen is palpated for masses, including, if spinal cord dysfunction is possible, a grossly enlarged bladder. Joint range of motion is assessed. If tick paralysis is suspected, the skin, particularly the scalp, should be thoroughly inspected for ticks.

41. Red flags In patients with weakness, the following findings are of particular concern: Weakness that becomes severe over a few days or less Dyspnea Inability to raise the head against gravity Bulbar symptoms (difficulty chewing, talking, and swallowing) Loss of ambulation Urinary retention or incontinence or fecal incontinence

42. Interpretation of findings The history helps differentiate weakness from fatigue, (time course of the illness, and gives clues to the anatomic pattern of weakness Weakness: Patients typically complain that they cannot do specific tasks.(usually has a particular pattern in time, anatomy, or both) Fatigue: Fatigue reported as weakness tends to have no temporal pattern ( “tired all of the time”) or anatomic pattern

43. Weakness that becomes severe within minutes or less usually caused by severe trauma or stroke Sudden weakness, numbness, and severe pain localized to a limb are more likely caused by local arterial occlusion and limb ischemia Weakness that progresses steadily over hours to days caused by acute or subacute disorders (SCC, transverse myelitis, spinal cord ischemia or hemorrhage, GBS,muscle wasting, rhabdomyolysis, botulism, organophosphate poisoning).

44. The temporal pattern of symptom Weakness that progresses over weeks to months caused by subacute or chronic disorders (cervical myelopathy, most inherited and acquired polyneuropathies,MG, motor neuron disorders, acquired myopathies, most tumors). Weakness that fluctuates from day to day may be caused by multiple sclerosis and sometimes metabolic myopathies. Weakness that fluctuates over the course of a day may be caused by MG, Eaton-Lambert syndrome, or periodic paralysis.

45. The anatomic pattern of weakness Characterized by specific motor tasks that are difficult to do. Anatomic patterns suggest certain diagnoses: I. Proximal muscle weakness Impairs reaching upward ( combing hair, lifting objects over the head), ascending stairs, or getting up from a sitting position; this pattern is typical of inflammatory myopathies

46. II. Distal muscle weakness Impairs tasks such as stepping over a curb, holding a cup, writing, buttoning, or using a key; this pattern is typical of polyneuropathies and myotonic dystrophy. Many disorders (Chronic inflammatory demyelinating polyneuropathy, GBS, MG, radiculopathies, Eaton-Lambert syndrome) cause proximal and distal weakness, but one pattern may be more prominent at first.

47. III. Bulbar weakness Cause facial weakness, dysarthria, and dysphagia, with or without impairment of ocular movements; MG, Eaton-Lambert syndrome, or botulism, certain motor neuron disorders, ALS or progressive supranuclear bulbar palsy.

48. Investiagtions If patients have no abnormal clinical findings test results are unlikely to be abnormal. Testing practices vary widely. CBC, Electrolytes (including calcium and magnesium), Glucose, RFT, (TSH),(ESR), and hepatitis C serologic testing. If brain upper motor neuron dysfunction is suspected, MRI,CT is used when MRI testing is not possible ( in patients with a cardiac pacemaker). Cerebrospinal fluid (CSF) analysis

49. CSF analysis useful in patients with Guillain-Barré syndrome; albuminocytologic dissociation (high protein level with a normal white cell count) is almost pathognomonic. If myopathy is suspected (suggested by muscle weakness, muscle cramping, and pain), Muscle enzymes (creatine kinase (CK), aldolase, lactic dehydrogenase [LDH] may be measured. Elevated levels are consistent with myopathy but can also be high in neuropathies (reflecting muscle atrophy) and very high in ischemic rhabdomyolysis.

50. Regular crack cocaine use can also cause chronically moderately elevated CK levels (mean value, 400 IU/L). Genetic testing can help confirm certain hereditary myopathies. If motor neuron disorders (ALS) are suspected, tests include electromyography and nerve conduction studies

51. Testing for specific disorders may be needed: If findings suggest MG, an ice pack test and serologic testing ( acetylcholine receptor antibody levels , sometimes anti muscle specific tyrosine kinase antibodies) If findings suggest vasculitis, autoantibody testing If family history suggests a hereditary disorder, genetic testing

52. Managemnt principles Causes of muscle weakness are treated. For patients with life-threatening, acute weakness, ventilatory support may be needed. Physical and occupational therapy can help people adapt to permanent weakness and minimize loss of function, regardless of the cause.

53. References Hutchison clinical methods 24th edition Davidson principle and practice of medicine 24th edition MSD MANUAL professional version Ceil essential of medicine 10th edition.