Weakness and paralysis — Medicine Library

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Quick guide

Diagnostic approach

ABCDE survey
Targeted clinical evaluation
Serum glucose
CBC
CMP
Serum magnesium and phosphate
CPK
TFTs
Bedside pulmonary function testing
ABG analysis if respiratory involvement is suspected
See “Diagnostics for neuromuscular weakness” for additional tests based on clinical suspicion.

Management checklist

Acute stabilization for neuromuscular weakness as needed
IV access
Pulse oximetry
Cardiac telemetry
Airway management
Hemodynamic support
Neuroprotective measures for suspected intracranial pathology.
Consult neurology and/or neurosurgery for neurological emergencies.

Red flag features

Signs of airway compromise
Respiratory muscle weakness
Neurogenic shock
Rapidly progressive symptoms
Clinical features of acute ischemic stroke
Signs of elevated ICP
Cerebral herniation syndromes

Stabilize patients with red flag features before performing diagnostic studies.

Life-threatening causes

Stroke
Intracranial hemorrhage
Spinal cord compression
Guillain-Barré syndrome
Myasthenic crisis
Botulism
Hyperkalemia
Cerebral herniation syndromes
Cholinergic poisoning

Summary

Weakness is a common symptom that can occur in a wide variety of conditions. In medical settings, “weakness” is best used to refer to decreased strength specifically attributable to neuromuscular abnormalities, rather than to systemic abnormalities of energy and metabolism. Degree of neurological weakness ranges from paresis (mild to moderate) to paralysis (severe or complete). The approach to patients with weakness requires careful clinical evaluation, including a detailed history and physical examination focusing on neurological examination and muscle strength grading. Specific patterns (e.g., acute vs. chronic, upper motor neuron vs. lower motor neuron) can help narrow down the etiology. Aggravating and alleviating factors, associated symptoms, and exposure history can often provide clues to a specific diagnosis. Diagnostic testing is guided by clinical evaluation and includes routine laboratory studies, targeted testing for specific neuromuscular disorders, neuroimaging, and electrodiagnostic studies. Specialist evaluation, e.g., by a neurologist, is often required. The management of weakness or paralysis varies significantly depending on the underlying cause and acuity of presentation and ranges from immediate respiratory support to supportive care, rehabilitation, and long-term pharmacotherapy.

See “Malaise and fatigue” for a more general approach not limited to neuromuscular causes.

Definitions

The following terms have imprecise definitions, and their usage can vary and overlap in both medical and lay contexts. [2]

Weakness: a lack of strength in the body or a body part
- In medical contexts, “weakness” is best reserved for describing neuromuscular weakness.
- Usage varies in the literature and in lay contexts; the term “generalized
  weakness” may also signify: [2][3][4]
  
  Malaise, fatigue, lethargy, or asthenia (See “Malaise and fatigue.”)
  
  Disability, exercise intolerance, or functional decline
  
  Related symptoms, e.g., muscle pain, incoordination, altered mental status, presyncope
Muscle fatigue: inability to continue a physical task after multiple repetitions
[4]
- Can be physiological (e.g., after excessive activity)
- Can occur pathologically in patients with neuromuscular weakness (e.g., myasthenia gravis, myopathy)
- See “Malaise and fatigue” for other types of fatigue.
Neuromuscular weakness
[5]
- Impairment in motor function (e.g., limitation in strength and/or range of motion) attributable to abnormalities in any of the following:
  
  Muscle structure and function
  
  Neurons
  
  Neuromuscular junction
- Can be generalized or localized, unilateral or bilateral, progressive or intermittent
- Most often measurable (e.g., using muscle strength grading)
  
  Paresis: mild to moderate degree of muscle weakness
  
  Paralysis: severe or complete loss of active muscle movement [6]

Clarify the intended meaning of potentially imprecise reported symptoms (e.g., weakness or fatigue) to avoid misdiagnosis, miscommunication, and unnecessary investigations.

Etiology

Several causes of neuromuscular weakness can have overlapping effects on muscles, neurons, and the neuromuscular junction. In extreme cases, they can cause paralysis. See “Malaise and fatigue” for non-neuromuscular causes of generalized weakness.

Muscular [2][7][8]

Acquired
- Sarcopenia and deconditioning (can coexist with frailty)
- Rhabdomyolysis
- Drug-induced myopathy; drugs associated with myopathy include: [4][7]
  
  Corticosteroids: See “Steroid-induced myopathy.”
  
  Statins: See “Statin myopathy.”
  
  Antineoplastics or antimetabolites, e.g., vincristine, hydroxyurea, colchicine
  
  Antiarrhythmics, e.g., procainamide, amiodarone
  
  Antivirals, e.g., interferon alpha, lamivudine, zidovudine (see “Zidovudine-induced myopathy.”)
  
  Antibiotics: e.g., fluoroquinolones, sulfonamides
  
  Recreational drugs: e.g., cocaine (see “Cocaine-induced myopathy.”)
- Critical illness myopathy
- Cushing syndrome
- Hypothyroid myopathy
- Acute alcohol-induced myopathy
- Inflammatory myopathies, e.g., dermatomyositis, polymyositis, inclusion body myositis
- See also “Differential diagnoses of myopathies.”
Hereditary
- Duchenne muscular dystrophy
- Becker muscular dystrophy
- Limb-girdle muscular dystrophy
- Facioscapulohumeral muscular dystrophy
- Myotonic syndromes, e.g., myotonic dystrophy
- Periodic paralysis (can also be acquired)

Neuromuscular junction (NMJ) [2][7]

Autoimmune: myasthenia gravis
Paraneoplastic: Lambert-Eaton myasthenic syndrome (LEMS)
Toxic
- Botulism
- Cholinergic poisoning, e.g., organophosphates
- Tick paralysis
- Snake envenomation

Lower motor neuron (LMN) [2][7][8]

Infectious
- Poliomyelitis
- Diphtheria
Autoimmune: Guillain-Barré syndrome (often post-infectious)
Inflammatory: chronic inflammatory demyelinating polyneuropathy (CIDP)
Hereditary
- Spinal muscular atrophy
- Hereditary motor sensory neuropathy
Others
- Progressive muscular atrophy (early)
- Critical illness polyneuropathy
- Alcoholic polyneuropathy
- Diabetic neuropathy
- Motor deficits are rare in drug-induced
  peripheral neuropathy but can occur with:
  [9]
  
  Chemotherapy-induced peripheral neuropathy
  
  Amiodarone
  
  Metronidazole
  
  Leflunomide
  
  Biological agents

Upper motor neuron (UMN) and CNS [4][7]

Structural
[7]
- TBI
- Spinal cord injury
- Brain tumor
- Spinal tumor
- Spinal stenosis
Vascular
- Stroke
- Anterior spinal artery syndrome
Inflammatory
- Multiple sclerosis (MS)
- Acute disseminated encephalomyelitis
- Transverse myelitis
Metabolic: central pontine myelinolysis
Congenital or hereditary
- Cerebral palsy
- Hereditary spastic paraplegia
- Subacute combined degeneration of spinal cord

Mixed syndromes [7]

Mixed
UMN and
LMN effects
- Amyotrophic lateral sclerosis (ALS)
- Progressive muscular atrophy (late stages)
Mixed
CNS and
PNS effects
- Systemic diseases (e.g., diabetic neuropathy, lupus) [10][11]
- Neuroborreliosis
- Vitamin B₁₂ deficiency
- Paraneoplastic syndromes
- Heavy metal poisoning, e.g., lead poisoning, mercury poisoning
- Cholinergic poisoning
- Amyloidosis
- Puffer fish poisoning

Electrolyte disturbances [7]

Can affect neurons and/or myocytes.

Hypokalemia or hyperkalemia
Hypocalcemia or hypercalcemia
Hyponatremia or hypernatremia
Hypomagnesemia or hypermagnesemia
Hypophosphatemia or hyperphosphatemia

Initial management

Approach [2][7]

Identify red flags in neuromuscular weakness.
Provide acute stabilization for neuromuscular weakness.
Exclude life-threatening mimics of neuromuscular weakness.
Ascertain the onset of symptoms to narrow the diagnosis.
- See “Acute causes of neuromuscular weakness.”
- See “Chronic causes of neuromuscular weakness.”
Localize the lesion on
neurological examination, e.g.:
- UMN signs vs. LMN signs
- Weakness patterns and associated lesions

Red flags in neuromuscular weakness [2]

These suggest an acutely life-threatening cause that requires urgent intervention:

Signs of airway compromise (especially bulbar palsy)
Signs of respiratory muscle weakness
Neurogenic shock
Rapidly progressive neurological symptoms, e.g., ascending paralysis
Clinical features of acute ischemic stroke
Signs of elevated ICP
Cerebral herniation syndromes

Classic respiratory distress signs (e.g., increased work of breathing) may be absent due to neuromuscular weakness. Signs may be limited to shallow breaths, low SpO₂, tachycardia, cyanosis, and/or altered mental status.

Acute stabilization for neuromuscular weakness [2][4]

Consider the following immediate steps in patients with red flags:

Airway management and ventilation
- Measure bedside PFTs.
- Predictors for the need for
  mechanical ventilation include:
  - Vital capacity < 15 mL/kg
  - Maximal inspiratory pressure less negative than - 30 cm H₂O
- Provide respiratory support as required (see “Ventilation strategy for neuromuscular weakness”).
Immediate hemodynamic support
Neuroprotective measures
ICP management
Consult neurology or neurosurgery urgently for definitive treatment of neurological emergencies (e.g., stroke or intracranial hemorrhage).
Consult ICU for patients requiring critical care(see “Disposition”).

Avoid succinylcholine as a paralytic agent for intubation in patients with suspected denervation or neuromuscular disorders to prevent life-threatening hyperkalemia. [2]

Intracranial hypertension can worsen during airway management. Follow the approach to intubating patients with increased ICP to avoid complications such as cerebral herniation. [2][12][13]

Clinical evaluation

Focused history [2][4][7]

Include the following:

Onset and duration: e.g., acute, subacute, chronic
Pattern: e.g., proximal, distal, symmetrical, asymmetrical
Progression: e.g., steady, episodic, fluctuating, ascending
Aggravating and alleviating factors: e.g., physical activity, rest
Associated neurological symptoms: e.g., sensory abnormalities, pain, tremors
Drug history: e.g., medications associated with myopathy
Past medical history: e.g., hypothyroidism
Exposures: e.g., toxins, tick bites, recent infections
Vaccination history: e.g., polio vaccination status, recent vaccines
Family history: e.g., muscular dystrophy, porphyria

Causes of transient or episodic weakness include multiple sclerosis, myasthenia gravis, and compressive peripheral neuropathies. [4]

Ascending bilateral weakness is seen in Guillain-Barré syndrome and tick paralysis, while descending weakness is characteristic of botulism. [4]

Focused examination [2][7]

Thorough
neurological examination
- Grade muscle strength using the Medical Research Council scale.
- Identify patterns, e.g., UMN signs vs. LMN signs, proximal vs. distal, symmetrical vs. asymmetrical.
- Pay close attention to:
  - Associated sensory deficits
  - Muscle tone, atrophy, and fasciculations
  - Reflexes (e.g., Babinski reflex)
  - Coordination and gait assessment
  - Cranial nerve examination
- Localize the lesion, if possible (see “Weakness patterns and associated lesions”).
Non-neurological clinical signs
- Skin rashes
- Cardiovascular abnormalities
- Cushingoid features
- Signs of dysautonomia
- Cholinergic toxidrome

In patients with isolated motor function abnormalities, consider ALS and botulism.

Difficulty performing a physical task on the first attempt suggests true neurological weakness. Difficulty sustaining repeated physical tasks suggests muscle fatigue. [4]

Lesion localization based on affected body parts

See also “Stroke symptoms by affected vessel,” “Lacunar syndromes,” “Brainstem syndromes,” and “Medullary syndromes.”

Weakness patterns and associated lesions [2]
		Lesion or disorder (most common)	Possible associated findings
Unilateral	Extremities and ipsilateral face	Contralateral cerebral cortex or internal capsule lesion (e.g., stroke, brain tumor)	Contralateral neglect or visual field deficit Ipsilateral sensory deficit Aphasia may be present.
	Extremities and contralateral face	Brainstem lesion (e.g., vertebrobasilar insufficiency, demyelination)	Cerebellar dysfunction Nystagmus Cranial neuropathy, e.g., diplopia, bulbar palsy Ipsilateral sensory deficit
	Extremity only (no facial involvement)	Contralateral focal motor cortex lesion (e.g., lacunar stroke) Incomplete spinal cord injury (e.g., Brown-Séquard syndrome) Peripheral nerve lesion	Motor cortex lesion or spinal cord lesion: UMN signs Brown-Séquard syndrome: ipsilateral proprioception, vibration, and fine touch sensory deficit, contralateral pinprick sensory deficit below motor lesion Peripheral nerve lesion: LMN signs
	Face only (no extremities)	Facial nerve (e.g., Bell palsy) Brainstem lesion	Brainstem lesion: multiple cranial neuropathies
Bilateral	Lower extremities only	Spinal lesion (e.g., T-spine or L-spine spinal cord injury or compression, cauda equina syndrome) Peripheral neuropathy (early)	Anterior cord syndrome: pain and temperature sensory deficit below motor level Compressive spinal emergencies: bowel or bladder dysfunction Guillain-Barré syndrome: ascending paralysis
	Upper extremities only	C-spine central cord syndrome (e.g., C-spine hyperextension injury, syringomyelia)	Pinprick sensory deficit with sparing of light touch sensation
	All four extremities	C-spine complete spinal cord injury NMJ disorder (e.g., Guillain-Barré syndrome) Myopathy (e.g., inflammatory myopathies, muscular dystrophies, rhabdomyolysis) Peripheral neuropathy	Spinal cord injury: associated sensory deficits, UMN signs Guillain-Barré syndrome: ascending paralysis Peripheral neuropathy: distal weakness Dermatomyositis, polymyositis, and periodic paralysis: proximal weakness
	Primarily face	NMJ disorder (e.g., myasthenia gravis, early botulism)	Additional cranial neuropathies (not limited to CN VII), bulbar palsy Myasthenia gravis: muscle fatigue Botulism: progressive generalized weakness

Proximal symmetrical weakness is a classic finding of most myopathies. [4][7]

Asymmetrical weakness suggests focal lesions of the brain, spinal cord, or peripheral nerves rather than a systemic cause. [2][7]

Diagnosis

Routine studies [7]

Consider screening for common systemic conditions (e.g., CBC, renal function tests, LFTs, septic workup, TFTs).
Obtain targeted studies based on clinical evaluation findings, e.g.:
- Serum electrolytes: calcium, magnesium, phosphate
- Creatine kinase (CK): for muscle damage or myopathy
- CSF analysis: for infectious or inflammatory causes
- Neuroimaging and spinal imaging: for structural causes
- Serologies: e.g., AChR-Ab for myasthenia gravis, Lyme serology
- Further studies, e.g., HIV testing, diagnostics for Cushing syndrome

Advanced studies [7]

Seek specialist guidance (e.g., neurology).

Electrodiagnostic studies to assess nerve and muscle function [7]
Muscle biopsy for objective weakness with abnormal CK levels or electrodiagnostic studies
Genetic testing for suspected hereditary neuromuscular disorders, such as muscular dystrophies

Acute onset or rapidly progressive causes

Acute or rapidly progressive acquired causes of neuromuscular weakness or paralysis [2][4][7]
	Distinguishing clinical features	Diagnostics	Management
Myasthenic crisis [14][15]	Acute clinical features of myasthenia gravis, e.g., fatigable proximal weakness, ptosis, diplopia, bulbar dysfunction Respiratory failure	Diagnostics for myasthenia gravis, e.g., AChR-Ab Spirometry and respiratory muscle function testing Vital capacity	Respiratory support Steroids IVIg See “Myasthenic crisis.”
Guillain-Barré syndrome [16][17]	Symmetrical ascending weakness Sensory symptoms (e.g., numbness, tingling) Autonomic dysfunction (e.g., orthostatic hypotension) Loss of reflexes	CSF analysis Electrodiagnostic studies	IVIg Plasmapheresis Respiratory support See “Management of Guillain-Barré syndrome.”
Botulism	Symmetrical descending paralysis Dry mouth and blurred vision Difficulty speaking and swallowing	Identification of botulinum toxin in serum or stool EMG	Botulism antitoxin Respiratory support See “Botulism.”
Poliomyelitis	Asymmetrical proximal weakness and/or paralysis Fever, muscle pain Respiratory paralysis (in severe cases)	PCR for enterovirus or poliovirus RNA CSF analysis (pleocytosis)	Respiratory support See “Poliomyelitis.”
Stroke, intracranial hemorrhage, or traumatic brain injury (TBI)	Sudden onset of unilateral neurological deficits Symptoms depend on localization of the lesion: See “Pattern-based localization of weakness lesion.”	CT or MRI head	See “Acute management checklist for ischemic stroke.” See “Acute management checklist for intracerebral hemorrhage.” See “Acute management checklist for SAH.” See “Acute management checklist for SDH.” See “Initial management of TBI.”
Carotid or vertebral artery dissection	Carotid artery dissection: ipsilateral headache, partial Horner syndrome, cranial neuropathy Vertebral artery dissection: occipital headache, central Horner syndrome, vertigo, ataxia, bulbar dysfunction	CT or MR angiography	Antithrombotic agents Surgical therapy in severe cases
Meningitis	Meningitis triad	CSF analysis Blood cultures CT or MRI head	Empiric antimicrobial therapy See “Acute management checklist for meningitis.”
MS exacerbation	New or worsening visual, motor, and/or sensory symptoms lasting > 24 hours and not accompanied by infection or fever	MRI to identify new or enlarging lesions Infection workup	High-dose corticosteroids Plasmapheresis See “Treatment of MS.”
Compressive spinal emergencies	Sudden onset of severe back pain Neurological deficits below the level of the lesion, e.g., weakness in the extremities Bladder or bowel dysfunction	MRI spine Post-void residual	Emergency decompression surgery See “Management of compressive spinal emergencies.”
Spinal cord injury	Paralysis and anesthesia below the level of injury Loss of bowel or bladder control Respiratory difficulties (if high cervical injury)	CT or MRI spine Post-void residual	Spinal stabilization See “Treatment of spinal cord injury.”
Transverse myelitis	Motor and sensory dysfunction (e.g., paresis, paralysis) below lesion level Bladder or bowel dysfunction	MRI spine Post-void residual	High-dose IV corticosteroids See “Transverse myelitis.”
Tick paralysis	Symmetrical ascending weakness	Examination for an attached tick	Tick removal Supportive treatment, e.g., respiratory support
Acute intermittent porphyria	Severe abdominal pain Polyneuropathies, e.g., descending symmetrical weakness, patchy paresthesia Red-purple urine	Spot urine for heme precursor levels Routine laboratory studies and imaging are often normal.	Hemin therapy Glucose loading See “Management of acute porphyric attacks.”
Cholinergic poisoning	Proximal muscle weakness Other features of cholinergic toxidrome Respiratory failure due to paralysis	Clinical diagnosis See “Diagnostics for cholinergic poisoning” for supportive and confirmatory studies.	Atropine Oxime therapy Respiratory support See “Management of cholinergic poisoning.”

Subacute or chronic onset, or gradually progressive causes

Subacute, chronic, or gradually progressive acquired causes of neuromuscular weakness or paralysis [2][7]
	Distinguishing clinical features	Diagnostics	Management
Myasthenia gravis	Ptosis, diplopia, bulbar palsy Respiratory muscle weakness Worsens with movement repetition Improves with rest	AChR-Ab EMG	Cholinesterase inhibitors, immunosuppressants Thymectomy for thymoma See “Treatment of myasthenia gravis.”
LEMS	Proximal muscle weakness Improves with movement repetition Autonomic symptoms, e.g., xerostomia, constipation	EMG Anti-VGCC antibody	Paraneoplastic LEMS: treatment of the underlying malignancy Amifampridine
ALS	Asymmetrical progressive limb weakness Bulbar palsy Respiratory failure	EMG MRI	Riluzole and edaravone Respiratory support
Multiple sclerosis (MS)	Depends on location of the lesions, e.g., optic neuritis, UMN weakness, or cranial nerve palsies	MRI brain and spinal cord CSF analysis Evoked potentials See “McDonald Criteria.”	Disease-modifying MS therapy See “Treatment of MS.”
CIDP	Symmetrical weakness of both proximal and distal muscles Sensory involvement (e.g., paresthesias)	NCS CSF analysis	Corticosteroids Plasmapheresis, IVIg Immunosuppressants
Neuroborreliosis	Meningitis, encephalitis Facial palsy Sensory deficits	Lyme serology CSF analysis	Antibiotics See “Neuroborreliosis.”
Heavy metal poisoning	Exposure to metal (e.g., lead, arsenic, mercury) Clinical features vary by substance May include weakness, sensory disturbances, and autonomic dysfunction	Blood or urine tests	Chelation therapy Limiting further exposure See “Metal toxicity.”
Polymyositis	Progressive proximal muscle weakness Difficulty climbing stairs and standing from a seated position	Muscle biopsy Blood tests for muscle enzymes EMG	Glucocorticoids and immunosuppressive agents See “Treatment of inflammatory myopathies.”
Dermatomyositis	Skin rash, especially on the face and hands Progressive proximal muscle weakness Difficulty swallowing	Muscle biopsy Blood tests for muscle enzymes Autoantibody testing (e.g., anti-Jo-1 antibodies)
Becker muscular dystrophy	Onset in adolescence and early adulthood Slowly progressive muscle weakness Primarily affects the pelvis and legs	↑ CK level Genetic testing for dystrophin gene mutations	Glucocorticoids Physical therapy Respiratory support See “Muscular dystrophies” for details.
Myotonic dystrophy	Myotonia (distal > proximal) Cataracts, heart conduction defects, endocrine changes	↑ CK level EMG Genetic testing for DMPK gene mutations	Symptomatic treatment Monitoring for cardiorespiratory compromise Physical therapy

Subsequent management

Further evaluation

Consult a specialist as needed, e.g., neurology, rheumatology.
Consider the possibility of
somatic symptom disorder or
conversion disorder in patients with:

Extensive prior workup with no identifiable cause

Physical findings inconsistent with reported symptoms

See “Approach to patients with suspected somatic symptom and related disorders” for details.

Supportive care

Pain management
Fluid replacement
Supportive care for decreased mobility
- Decubitus ulcer prophylaxis
- VTE prophylaxis
- Urinary catheterization
Medical rehabilitation

Disposition

Admission is usually required for:
[2]
- Vascular CNS causes of weakness, e.g., stroke
- Severe or rapidly progressive LMN or muscular weakness, e.g., botulism, Guillain-Barré syndrome
- New UMN weakness, e.g., spinal cord injury, MS exacerbation
ICU admission is usually required for ascending paralysis, respiratory failure, airway compromise, and neurogenic shock.
Admission to a stroke center or neurocritical care unit may be indicated. [2]

Differential diagnoses

The following conditions can be conflated with or mistaken for neuromuscular weakness. For causes of neuromuscular weakness, see the “Etiology” section. See “Stroke mimics” for differential diagnoses of focal or diffuse neurological deficits. [2]

Potentially life-threatening mimics of neuromuscular weakness
- Hypoglycemia
- Shock, hypovolemia
- Infection, sepsis
- DKA
- Traumatic brain injury
- Acute heart failure
- Acute coronary syndrome
- Bradycardia
- Poisoning, e.g., with cellular toxins
Other general symptoms
- Malaise or fatigue
- Altered mental status and coma (e.g., due to sedative-hypnotic drug overdose)
- Presyncope
- Vertigo
- Functional decline
Other neurological symptoms
- Pain-induced motor dysfunction
- Incoordination or ataxia
Disorders of circulation and
oxygen delivery
- Dehydration
- Anemia or polycythemia

The differential diagnoses listed here are not exhaustive.

External Resources

References

Larson ST, Wilbur J. "Muscle Weakness in Adults: Evaluation and Differential Diagnosis.". Am Fam Physician. 101(2). :95-108. (2020)
Walls R, Hockberger R, Gausche-Hill M, Erickson TB, Wilcox SR. "Rosen's Emergency Medicine 10th edition- Concepts and Clinical Practice E-Book". Elsevier Health Sciences. (2022). ISBN: 9780323757904
Busl KM, Ropper AH. "Hospital Consultation for the Patient With Generalized Weakness". Continuum (Minneap Minn). 17. :1040-1062. (2011)
Ganti L, Rastogi V. "Acute Generalized Weakness". Emerg Med Clin North Am. 34(4). :795-809. (2016)
Jones MR, Urits I, Wolf J, et al. "Drug-Induced Peripheral Neuropathy: A Narrative Review". Curr Clin Pharmacol. 15(1). :38-48. (2020)
Ferris JK, Inglis JT, Madden KM, et al. "Brain and Body: A Review of Central Nervous System Contributions to Movement Impairments in Diabetes". Diabetes. 69(1). :3-11. (2019)
Appenzeller S, Costallat LTL, Cendes F. "Neurolupus". Arch Neurol. 63(3). :458. (2006)
Wendell LC, Levine JM. "Myasthenic Crisis". Neurohospitalist. 1(1). :16-22. (2011)
Gwathmey K, Burns T. "Myasthenia Gravis". Semin Neurol. 35(04). :327-339. (2015)
Walling AD, Dickson G. "Guillain-Barré syndrome". Am Fam Physician. 87(3). :191-7. (2013)
Leonhard SE, Mandarakas MR, Gondim FAA, et al. "Diagnosis and management of Guillain–Barré syndrome in ten steps". Nat Rev Neur. 15(11). :671-683. (2019)
American College of Surgeons and the Committee on Trauma. "ATLS Advanced Trauma Life Support". American College of Surgeons. (2018). ISBN: 9780996826235
Roberts JR. "Roberts and Hedges' Clinical Procedures in Emergency Medicine and Acute Care". Elsevier. (2018). ISBN: 9780323354783
Latimer KM, Gunther A, Kopec M. "Fatigue in Adults: Evaluation and Management". Am Fam Physician. 108(1). :58-69. (2023)
Khamees D, Meurer W. "Approach to Acute Weakness". Emerg Med Clin North Am. 39(1). :173-180. (2021)
Armour BS, Courtney-Long EA, Fox MH, et al. "Prevalence and Causes of Paralysis—United States, 2013". Am J Public Health. 106(10). :1855-1857. (2016)
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