Differentials
Guillain-Barre syndrome (GBS)
SIGNS / SYMPTOMS
Presents with ascending paralysis in 95% of cases.[58]
A history of preceding respiratory or gastrointestinal illness (Campylobacter jejuni in one third of cases) also suggests GBS.
The Miller Fisher variant of GBS is characterized by ophthalmoplegia, ataxia, and areflexia; only one fourth of such patients will demonstrate the extremity weakness seen in GBS cases.
INVESTIGATIONS
Lumbar puncture: GBS patients may display an increased cerebrospinal fluid (CSF) protein level, while in botulism, CSF results are normal.
Myasthenia gravis
SIGNS / SYMPTOMS
Patients with myasthenia gravis do not display autonomic instability.
INVESTIGATIONS
Nearly all patients with myasthenia gravis display autoantibodies against the acetylcholine receptor (AChR-Ab).[59]
Tick paralysis (Dermacentor)
SIGNS / SYMPTOMS
Excluded by physical exam, as the Dermacentor tick will still be attached in symptomatic patients.
Ticks are found most often on the scalp or neck, but may be attached in the axilla or perineum.
In contrast to patients with botulism, patients with tick paralysis report ascending (not descending) symptoms.
INVESTIGATIONS
Diagnosis is clinical.
Lambert-Eaton myasthenic syndrome (LEMS)
SIGNS / SYMPTOMS
LEMS is usually differentiated by increased strength with sustained contraction in affected patients.
INVESTIGATIONS
Most patients with LEMS have a characteristic electrophysiologic pattern that supports the diagnosis. The compound muscle action potential (CMAP) of resting muscle in patients with LEMS usually has a significantly reduced baseline amplitude.[59]
Following high-frequency (10-50 Hz) repetitive nerve stimulation (RNS) or brief maximal isometric muscle activation, there is a significant increment with a marked increase in the CMAP amplitude. This increase in the CMAP amplitude following high-frequency RNS or brief isometric exercise is referred to as postexercise or postactivation facilitation.
Organophosphate toxicity
SIGNS / SYMPTOMS
Acute toxicity is characterized by symptoms of cholinergic excess: bradycardia, lacrimation, salivation, bronchospasm, urination, emesis, and diarrhea.
Intoxication with a highly fat-soluble organophosphate may result in an intermediate syndrome. Affected patients present with neck weakness, decreased deep tendon reflexes, cranial nerve abnormalities, and proximal muscle weakness resembling botulism cases.
INVESTIGATIONS
Direct measurement of red blood cell acetylcholinesterase activity may be used, but most hospital laboratories are unable to perform this test. An assay for plasma cholinesterase activity can be performed. Symptoms in patients affected by organophosphate toxicity will respond to a trial of atropine in adults or children.
Magnesium toxicity
SIGNS / SYMPTOMS
Hypermagnesemia may result in muscle paralysis and loss of deep tendon reflexes.
As smooth muscle function is also impaired, patients may have decreased respiration and eventual apnea.
Patients with magnesium toxicity are often somnolent.
INVESTIGATIONS
Elevated magnesium levels.
Spinal muscular atrophy (SMA)
SIGNS / SYMPTOMS
SMA is an inherited disorder; there are various types affecting newborns to adults. Weakness onset is more prolonged compared with the more acute presentation of weakness in botulism. In the infantile type of SMA, weaknesses of eye muscles and anal sphincters are not typical features as they are with botulism.[60]
INVESTIGATIONS
Genetic testing for mutations associated with SMA is available.
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