Guillain-Barré syndrome physical examination
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, MBBS [2]
Overview
It is included in the wider group of peripheral neuropathies. The physical examination findings usually indicates features due to autonomic dysfunction and demyelination of peripheral nerves. Fluctuation in vitals can be seen and may present as hyper or hypothermia, hypo or hypertension, brady or tachycardia. Progressive, symmetric, bilateral, flaccid, ascending paralysis progressing over weeks to days time is the common finding. Hypotonia, hyporeflexia, areflexia can be seen.Sensory system may be involved but generally it is mild. Ataxia and difficulty in walking may be seen despite great muscle strength due to involvement of proprioception and oculoparesis.
Physical Examination
Physical examination of patients with Guillain Barre syndrome is usually remarkable for:
Appearance of the Patient
- Patients with Guillain Barre syndrome might have abnormal gait.[1]
Vital Signs
- Tachycardia or bradycardia
- Blood pressure disturbance[2]
Skin
- Skin examination of patients with Guillain Barre syndrome is usually normal.
- We might see evidence of recent chicken pox disease.
HEENT
- Extra-ocular movements may be abnormal (ophthalmologist).[1]
- Ophthalmoscopic exam may be abnormal with findings of papilledema.[3]
- Hearing acuity may be reduced.[4]
- facial myokymia (Involuntary facial movement)[5]
- vocal cord paralysis (Difficulty speaking)[6]
Neck
- We might see some Lymphadenopathy because of prior infection with EBV or CMV.
- Using accessory muscle for breathing in severe cases.
Lungs
- Pulmonary examination of patients with Guillain barre syndrome is usually normal.
Heart
- Cardiovascular examination of patients with Guillain Barre syndrome is usually normal.
Abdomen
- Abdominal examination of patients with Guillain Barre syndrome is usually normal.
Back
- Back examination of patients with Guillain Barre syndrome is usually normal.
Genitourinary
- Evidences of urinary retention may be present.[2]
Neuromuscular
- Neuromuscular examination of patients with [disease name] is usually normal.
OR
- Patient is usually oriented to persons, place, and time
- Altered mental status
- Glasgow coma scale is ___ / 15
- Clonus may be present
- Hyperreflexia / hyporeflexia / areflexia
- Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
- Muscle rigidity
- Proximal/distal muscle weakness unilaterally/bilaterally
- ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
- Unilateral/bilateral upper/lower extremity weakness
- Unilateral/bilateral sensory loss in the upper/lower extremity
- Positive straight leg raise test
- Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
- Positive/negative Trendelenburg sign
- Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
- Normal finger-to-nose test / Dysmetria
- Absent/present dysdiadochokinesia (palm tapping test)
Extremities
- Extremities examination of patients with [disease name] is usually normal.
OR
- Clubbing
- Cyanosis
- Pitting/non-pitting edema of the upper/lower extremities
- Muscle atrophy
- Fasciculations in the upper/lower extremity
Common symptoms
Common symptoms of Guillain Barre syndrome include:
- Most of Guillain Barre syndrome cases can be diagnosed based on partially symmetrical ascending weakness and paralysis.
- Can cause sensory symptoms such as tingling and paresthesia.[7]
- Because of nerve inflammation, in the acute phase of GBS patients complain of pain.[8]
- Some of the features may be specific to different subgroups of GBS.
- Acute inflammatory demyelinating polyneuropathy:[2]
- It affects lower extremities first and then involves upper extremities, trunk, neck and cranial nerves.
- It can involve sensory neurons.
- Deep sensation is the most affected sense.
- It causes areflexia
- In AIDP we may see autonomic involvement such as changes in heart rate and blood pressure and urinary retention.
- Acute motor axonal neuropathy/Acute motor and sensory axonal neuropathy:[9][10]
- Can causes hyperreflexia.
- Autonomic dysfunction in absent or mild.
- AMSAN can causes severe type of GBS with slow recovery
- Miller Fisher syndrome[1]
- This type of GBS causes ophthalmoplegia.
- The reflexes are absence.
- There is gait abnormalities (Ataxia).
- Acute inflammatory demyelinating polyneuropathy:[2]
Less Common Symptoms
Less common symptoms of Guillain Barre syndrome include:
- Symptoms of papilledema such as
- Head ache
- Visual disturbance[3]
- Involuntary facial movement (facial myokymia)[5]
- Hearing loss[4]
- Difficulty speaking (vocal cord paralysis)[6]
- Mental status changes[11]
References
- ↑ 1.0 1.1 1.2 Mori M, Kuwabara S, Fukutake T, Yuki N, Hattori T (April 2001). "Clinical features and prognosis of Miller Fisher syndrome". Neurology. 56 (8): 1104–6. PMID 11320188.
- ↑ 2.0 2.1 2.2 Template:Victor, M., 2001. Diseases of spinal cord peripheral nerve and muscle. Principles of Neurology
- ↑ 3.0 3.1 JOYNT RJ (January 1958). "Mechanism of production of papilledema in the Guillain-Barre syndrome". Neurology. 8 (1): 8–12. PMID 13493684.
- ↑ 4.0 4.1 Nelson KR, Gilmore RL, Massey A (August 1988). "Acoustic nerve conduction abnormalities in Guillain-Barré syndrome". Neurology. 38 (8): 1263–6. PMID 3399076.
- ↑ 5.0 5.1 Mateer JE, Gutmann L, McComas CF (March 1983). "Myokymia in Guillain-Barré syndrome". Neurology. 33 (3): 374–6. PMID 6681885.
- ↑ 6.0 6.1 Panosian MS, Quatela VC (February 1993). "Guillain-Barré syndrome presenting as acute bilateral vocal cord paralysis". Otolaryngol Head Neck Surg. 108 (2): 171–3. doi:10.1177/019459989310800211. PMID 8441543.
- ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
- ↑ Moulin DE, Hagen N, Feasby TE, Amireh R, Hahn A (February 1997). "Pain in Guillain-Barré syndrome". Neurology. 48 (2): 328–31. PMID 9040715.
- ↑ Kuwabara S, Ogawara K, Koga M, Mori M, Hattori T, Yuki N (August 1999). "Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody". J. Neurol. Neurosurg. Psychiatry. 67 (2): 180–4. PMC 1736477.
- ↑ Kuwabara S, Nakata M, Sung JY, Mori M, Kato N, Hattori T, Koga M, Yuki N (July 2002). "Hyperreflexia in axonal Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis". J. Neurol. Sci. 199 (1–2): 89–92. PMID 12084449.
- ↑ Cochen V, Arnulf I, Demeret S, Neulat ML, Gourlet V, Drouot X, Moutereau S, Derenne JP, Similowski T, Willer JC, Pierrot-Deseiligny C, Bolgert F (November 2005). "Vivid dreams, hallucinations, psychosis and REM sleep in Guillain-Barré syndrome". Brain. 128 (Pt 11): 2535–45. doi:10.1093/brain/awh585. PMID 16000335.