Differentials

Drug-induced dystonias, for example, phenothiazines

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Features may include torticollis, retrocollis, trismus, glossopharyngeal dystonia, opisthotonus, and often deviation of the eyes. Tetanus is not associated with ocular deviation.

A compatible drug history would support a diagnosis of drug-induced dystonia.

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Anticholinergic agents such as procyclidine or benztropine usually ameliorate drug-induced dystonias but have no effect on tetanus.

Strychnine poisoning

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Strychnine is a white, odorless, poisonous powder that can be taken by mouth, inhaled (e.g., mixed with cocaine/heroin), or injected intravenously in solution. It is a competitive antagonist of the inhibitory neurotransmitter glycine at receptors in the spinal cord, brainstem, and higher centers.

Symptoms of poisoning usually appear within 15 to 60 minutes of ingestion and include heightened awareness, agitation, restlessness, painful muscular spasms and rigidity, trismus, opisthotonus, and hypersensitivity to stimuli.[44] Respiratory muscle spasm can cause respiratory arrest.

Ingestion of large amounts can lead to painful generalized convulsions, during which the patient retains consciousness.

Patient may give a history of snorting street drugs or deliberate/accidental ingestion of strychnine, which may be present in pesticide preparations, particularly rat poison.

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Blood, urine, and tissue assays for strychnine should be requested in suspected poisoning or when apparent tetanus presents in a fully immunized patient or in the absence of an antecedent tetanus-prone injury.

Neuroleptic malignant syndrome

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An idiosyncratic reaction to antipsychotic medication, featuring rapid onset of hyperthermia, muscular rigidity, extrapyramidal signs, autonomic dysfunction, mutism, confusion, and even coma. Tremor and urinary incontinence may be present.

The condition is attributed to dopamine receptor blockade. The patient's drug history should indicate a possible cause. All classes of antipsychotic agents (dopamine D2 receptor antagonists) have been implicated, as well as non-antipsychotic agents, which block central dopamine pathways such as metoclopramide.

It is more likely to develop after initiation of antipsychotic therapy or an increase in dose, but can occur at any time during treatment, even years after starting therapy. Withdrawal of anti-Parkinson medication can also precipitate the syndrome.

Altered mental status is less common in tetanus.

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Clinical diagnosis.

Stiff person syndrome

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Severe progressive muscle rigidity of the trunk and limbs with superimposed spasms, which may be triggered by voluntary movements, external stimuli, or emotional stress.

Trismus and facial spasms are absent.

The patient may experience unprotected falls like a tin soldier.

Symptom onset is typically between the ages of 30 and 50 years. Most cases begin insidiously and progress over years, although some can develop over weeks.

Patients often have other autoimmune conditions.

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Glutamic acid decarboxylase autoantibodies in 60% of patients. Electromyogram reveals a characteristic abnormality. There is a rapid response to diazepam.

Hypocalcemia

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Perioral and peripheral numbness/tingling and muscle cramps, which may progress to carpopedal spasm.

There may be a history of irritability, confusion, reduced intellectual capacity, or depression. Seizures can occur as well as movement disorders, for example, choreoathetosis, dystonic spasms, parkinsonism, and hemiballismus.

Wheezing may arise due to bronchospasm. Cardiac abnormalities include arrhythmias and congestive heart failure.

Clinical signs of chronic hypocalcemia may be present, for example, brittle nails, coarse hair/alopecia, dry skin.

The patient's history, drug history, and physical examination may suggest an underlying cause for hypocalcemia. Bisphosphates, anticonvulsants, foscarnet, and cisplatin can lead to hypocalcemia.

It may be possible to elicit Chvostek and Trousseau signs, which are suggestive of hypocalcemia.

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Hypocalcemia is confirmed by laboratory measurement of ionized calcium. ECG may show prolonged QT interval. Further investigations may establish the underlying cause: phosphate, alkaline phosphatase, magnesium, PTH, 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D, renal and liver function, amylase, etc.

Dental/parapharyngeal/parotid/tonsillar infection or diphtheria

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These infections can cause trismus without spasms or generalization.

Localized swelling, tenderness, or exudate may be apparent.

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Radiologic imaging may confirm deep abscesses.

Meningitis

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Meningitis and meningoencephalitis can produce trismus, rigidity, seizures, and opisthotonus, but risus sardonicus is absent.[25]

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The cerebrospinal fluid findings differentiate between these conditions and tetanus. The protein may be slightly elevated in tetanus, but the cell count is normal.[25]

Generalized seizures in children

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The differentiation between seizures and tetanus may be particularly difficult in neonates. However, in epilepsy consciousness is impaired, and the muscles are often hypotonic and flaccid in the postictal state.[25]

INVESTIGATIONS

Abnormal electroencephalogram in epilepsy.

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