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Approach to Acute Weakness

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Ehab Eshtaya

on 20 March 2013

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Transcript of Approach to Acute Weakness

Approach to Acute Weakness in Adults presenting to The Emergency Department Ehab Eshtaya, MD Acute
Weakness Paresis Shock /
Relative ischemia Inflammatory Metabolic/
endocrine Psychogenic Paralysis is the loss of voluntary movement because of interruption of one of the motor pathways at any point from the cerebrum to the muscle fiber.

Paresis is a lesser degree of paralysis. Cardiogenic Obstructive Volume depletion Impaired delivery Infection Cancer Rheumatologic Allergy Cerebral Cortex Subcortical tract Brain Stem Spinal Cord corona radiata
posterior limb of the internal capsule Medulla Decussation Transition of the UMN
to LMN - anterior horn "The Thinkers" Case 1

32y male with progressive (6 days), bilateral muscle weakness (lower extremity > upper extremity), and paresthesia x 4 limbs, accompanied by absent deep tendon reflexes. Bladder retention.

Vitals: Normal
GCS: 15/15 Upper Motor
Neuron Lower Motor
Neuron Neuromuscular
Junction Muscular Clinical Findings

Strength - diminished to absent
Reflexes - increased*
Sensory - Variable
Tone - Increased (spasticity)
Gait - Spastic
Babinski - up going plantar Perceived
Weakness Hypothyroid
Adrenal
Azotemia
Sodium
Ethanol
Medications Hyperthyroid *
Glucose *
Potassium *
Calcium
Phosphate
Magnesium
Ethanol
Medications Anxiety / Depression

Fibromyalgia

Chronic fatigue Syndrome

Conversion Disorder *

Malingering Myofibril
Muscle fiber
Muscle fascicle
Muscle
Tendon Perceived weakness - The patient feels that more energy is required to exert a given amount of force, when in fact the actual muscle strength is normal. Distributive Step 1 Assess ABC
Assess Level of Consciousness Manage accordingly Reversible
Causes Perceived Paresis Shock

Severe Metabolic

Severe Endocrine Massive cerebral stroke

Thalamic Stroke/lesion

Brainstem stroke/lesion

Cord inflammation/compression

Guillen Barre Syndrome

Tick Paralysis

Organophosphate toxicity

Botulism

Myasthenic Crisis Compromised Step 2 Step 3 Perceived Weakness vs Paresis Perceived Correct underlying
Cause and reevaluate Normal Paresis Unilateral vs Bilateral Unilateral UMN LMN Radiculopathy

Plexopathy

Peripheral nerve injury/entrapment Physical Exam* Cortical - often associated with aphasia, neglect, visual field deficit

Subcortical - often purely motor. Ataxia and 'shaking hand'.

Brainstem - associated with CN deficit (contralateral)

Cord - Rarely pure motor; often associated with sensory level and bowel/bladder dysfunction. Ischemia

Hemorrhage

Tumor

Infections (Polio/ West Nile)

Inflammatory (MS / transverse myelitis)

Migraine - hemiplegic (rare)

Post-ictal (Todd's) paralysis Differential Diagnosis Differential Diagnosis Radiculopathy
- Direct compression/impingement
- Lyme disease (late in disease)

Plexopathy
- Direct compression/impingement
- Tick Paralysis*

Neuropathy (poly/mono)
- Guillain Barre
- Diphtheria
- Arsenic / hexane / Thallium / mercury / lead / Tick exotoxin
- vasculitis/sarcoidosis
- Porphyria / paraneoplastic Botulism / Snake Venom

Hypocalcemia / Hypermagnesemia

Organophosphate / Carbamates poisoning

Myasthenia Gravis/ Myasthenic Crisis

Tick Paralysis* (LMN) Cortical / Subcortical - Should have been identified on Step 1.

Brainstem - associated with CN deficit (potentially life threatening)

Cord - Rarely pure motor; often associated with sensory level and cord level plegia +/- bowel / bladder signs. Step 5 LMN Signs - LE > UE, sensory symptoms +/- autonomic dysfunction? Step 4 UMN vs non - UMN Yes Guillain Barre Tick Paralysis CSF - Abnormal
Objective sensory deficit
Subacute course
Always bilateral
No ticks on PE
bladder/bowel common CSF - Normal
Normal sensory exam
Acute course
Variable (single limb to full)
Tick present on PE No Step 7 Weakness Proximal > Distal +
No sensory signs +/- myalgia Yes Muscular Pathology No Step 6 *Early Oculobulbar weakness
Fatigable on exertion
Proximal > distal weakness *Consider Toxins:
Arsenic poisoning / hexane / Thallium / mercury / lead Yes Neuromuscular Junction
Disorders Unilateral UMN Bilateral Non - UMN Case 2

46y female with acute bilateral facial muscle weakness, ptosis, dysarthria, followed by bilateral upper limb weakness. Blurred vision but no other sensory symptoms. No spasticity, decrease deep tendon reflexes.

Vitals: Normal
GCS: 15/15 Clinical Findings

Strength - decreased (LE > UE)
Reflexes - decreased to absent
Sensory - Very common*
Tone - decreased to flaccid
Gait - Normal to unsteady*
Babinski - down going plantars
Other - Autonomic dysfunction "I feel weak" Clinical Findings

Strength - LE > UE > Oculobulbar
Reflexes - Normal*
Sensory - Normal
Tone - Normal
Babinski - down going plantar
Other - Muscle fatigue with repetition Differential Diagnosis Clinical Findings

Strength - Decreased (prox > dist)
Reflexes - Depends on severity
Sensory - Normal
Tone - Normal
Babinski - Down going plantar
Other - Tenderness on palpation* Inflammatory Myopathy

Rhabdomyolisis Differential Diagnosis Step 1 Assess ABC
Assess Level of Consciousness Manage accordingly Reversible
Causes Perceived Paresis Shock

Severe Metabolic

Severe Endocrine Massive cerebral stroke

Thalamic Stroke/lesion

Brainstem stroke/lesion

Cord inflammation/compression

Guillen Barre Syndrome

Tick Paralysis

Organophosphate toxicity

Botulism

Myopathic Crisis Compromised Step 2 Step 3 Perceived Weakness vs Paresis Perceived Correct underlying
Cause and revaluate Normal Paresis Unilateral vs Bilateral Unilateral UMN LMN Radiculopathy

Plexopathy

Peripheral nerve injury/entrapment Physical Exam* Cortical - often associated with aphasia, neglect, visual field deficit

Subcortical - often purely motor. Ataxia and 'shaking hand'.

Brainstem - associated with CN deficit (contralateral)

Cord - Rarely pure motor; often associated with sensory level and bowel/bladder dysfunction. Cortical / Subcortical - Should have been identified on Step 1.

Brainstem - associated with CN deficit (potentially life threatening)

Cord - Rarely pure motor; often associated with sensory level and cord level plegia +/- bowel / bladder signs. Step 5 LMN Signs - LE > UE, sensory symptoms, and dysautonomia Step 4 UMN vs non - UMN Yes Guillain Barre Tick Paralysis CSF - Abnormal
Objective sensory deficit
Subacute course
Always bilateral
No ticks on PE
bladder/bowel common CSF - Normal
Normal sensory exam
Acute course
Variable (single limb to full)
Tick present on PE No Step 7 Weakness Proximal > Distal +
No sensory signs +/- myalgia Yes Myositis (inflamatory vs viral)
Alcoholic myopathy

- Asses heart function * Muscular Pathology No Step 6 *Early Ocular and Bulbar weakness
Fatiguibale on excertion
Proximal > distal weakness *Consider Toxins:
Arsenic poisoning / hexane / Thallium / mercury / lead Yes Neuromuscular Junction
Disorders Unilateral UMN Bilateral Non - UMN Oculobulbar - exit on the
contralateral side. Aknowledgments

Dr Fisher - Internal Medicine Staff
Dr Smyth - Neurology Staff
Dr Lefebvre - Emergency Medicine Objectives Gain an algorithmic approach to 'acute weakness' as a presenting complaint in the Emergency Department

Basic understanding of the clinical presentation and differential diagnosis for the different components of the Neuromuscular pathway

Highlights of Guillain Barre Syndrome and Botulism as example of LMN and NMJ disorders. - Acute monophasic illness provoked by previous infection
- Rapidly progressive secondary to autoimmune process
- Demyelinating / Axonal Polyneuropathy Cardinal clinical features of GBS

- Progressive, symmetric muscle weakness
- Absent or depressed deep tendon reflexes.
- Respiratory failure in about 30 percent,
- Dysautonomia occurs in 70% of patients.
- Progresses over 2 weeks on average
- Facial weakness (50%) ocular muscles (15%)
- Often a prominent severe back pain
- Sensory disturbance in 80% (often mild)
- Has multiple variants (AIDP, Miller Fisher, AMAN) Guillain Barre Syndrome (GBS) Investigations

LP - Elevated protein count with normal WBC (albuminocytologic dissociation)

EMG/NCS - Evidence of either demyelinating or axonal neuropathy (depends on the variant)

Systemic Antibodies - GQ1b useful for Miller Fisher variant; otherwise of no clinical utility. Treatment

Supportive Therapy
Intubate if impending respiratory failure
Analgesia for neuropathic pain (50%)
Plasma Exchange or IVIG
No role for steroids Prognosis

Clinical course with no treatment
- Progression of disease up to 2 weeks
- Plateau for 2 weeks
- Recovery 'weeks' to 'months'

Long term
- 85% complete recovery
- 10% delayed and incomplete recovery
- 5% die
- 10% recurrence Step 1 Assess ABC
Assess Level of Consciousness Manage accordingly Reversible
Causes Perceived Paresis Shock

Severe Metabolic

Severe Endocrine Massive cerebral stroke

Thalamic Stroke/lesion

Brainstem stroke/lesion

Cord inflammation/compression

Guillen Barre Syndrome

Tick Paralysis

Organophosphate toxicity

Botulism

Myopathic Crisis Compromised Step 2 Step 3 Perceived Weakness vs Paresis Perceived Correct underlying
Cause and revaluate Normal Paresis Unilateral vs Bilateral Unilateral UMN LMN Radiculopathy

Plexopathy

Peripheral nerve injury/entrapment Physical Exam* Cortical - often associated with aphasia, neglect, visual field deficit

Subcortical - often purely motor. Ataxia and 'shaking hand'.

Brainstem - associated with CN deficit (contralateral)

Cord - Rarely pure motor; often associated with sensory level and bowel/bladder dysfunction. Cortical / Subcortical - Should have been identified on Step 1.

Brainstem - associated with CN deficit (potentially life threatening)

Cord - Rarely pure motor; often associated with sensory level and cord level plegia +/- bowel / bladder signs. Step 5 LMN Signs - LE > UE, sensory symptoms, and dysautonomia Step 4 UMN vs non - UMN Yes Guillain Barre Tick Paralysis CSF - Abnormal
Objective sensory deficit
Subacute course
Always bilateral
No ticks on PE
bladder/bowel common CSF - Normal
Normal sesnory exam
Acute course
Variable (single limb to full)
Tick present on PE No Step 7 Weakness Proximal > Distal +
No sensory signs +/- myalgia Yes Myositis (inflamatory vs viral)
Alcoholic myopathy

- Asses heart function * Muscular Pathology No Step 6 *Early Ocular and Bulbar weakness
Fatigable on exertion
Proximal > distal weakness *Consider Toxins:
Arsenic poisoning / hexane / Thallium / murcury / lead Yes Neuromuscular Junction
Disorders Unilateral UMN Bilateral Non - UMN Botulism is a neuroparalytic syndrome resulting from the action of a neurotoxin elaborated by the bacterium Clostridium botulinum, .a heterogeneous group of gram-positive, rod-shaped, spore-forming, obligate anaerobic bacteria. Cardinal clinical features of Botulism

- Acute onset of bilateral cranial neuropathies
- Symmetric descending weakness
- Absence of fever
- The patient remains responsive
- No sensory deficit, except for blurred vision
- Heart Rate normal to slow
- Five forms of botulism exist, including food borne botulism, infant botulism, wound botulism, adult enteric infectious botulism, and inhalation botulism Botulism Investigations

Generally not applicable; clinical diagnosis

Non specific blood markers

spores and/or toxin can be isolated Treatment

Supportive Therapy
Intubate if impending respiratory failure
Anti-toxin (Equine serum botulism antitoxin and Human-derived botulinum immune globulin)
Pen G if wound infection (metronidazole if Pen allergy Prognosis

Requires 1 - 3 months of hospitalization regardless of the type of botulism
Ventilator support in 20-30%

Long term
- 5 - 8% mortality
- 1% newborn mortality
- long term sequelae of perceived weakness 25% ?
Full transcript