Differentials
Drug-induced dystonias, for example, phenothiazines
SIGNS / SYMPTOMS
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.
INVESTIGATIONS
Anticholinergic agents such as procyclidine or benzatropine usually ameliorate drug-induced dystonias but have no effect on tetanus.
Strychnine poisoning
SIGNS / SYMPTOMS
Strychnine is a white, odourless, 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 centres.
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 hyper-sensitivity to stimuli.[42] Respiratory muscle spasm can cause respiratory arrest.
Ingestion of large amounts can lead to painful generalised 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.
INVESTIGATIONS
Blood, urine, and tissue assays for strychnine should be requested in suspected poisoning or when apparent tetanus presents in a fully immunised patient or in the absence of an antecedent tetanus-prone injury.
Neuroleptic malignant syndrome
SIGNS / SYMPTOMS
An idiosyncratic reaction to antipsychotic medicine, 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 medicine can also precipitate the syndrome.
Altered mental status is less common in tetanus.
INVESTIGATIONS
Clinical diagnosis.
Stiff person syndrome
SIGNS / SYMPTOMS
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 suffer 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.
INVESTIGATIONS
Glutamic acid decarboxylase autoantibodies in 60% of patients. Electromyogram reveals a characteristic abnormality. There is a rapid response to diazepam.
Hypocalcaemia
SIGNS / SYMPTOMS
Peri-oral 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 hypocalcaemia 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 hypocalcaemia. Bisphosphates, anticonvulsants, foscarnet, and cisplatin can lead to hypocalcaemia.
It may be possible to elicit Chvostek and Trousseau signs, which are suggestive of hypocalcaemia.
INVESTIGATIONS
Hypocalcaemia is confirmed by laboratory measurement of ionised 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
SIGNS / SYMPTOMS
These infections can cause trismus without spasms or generalisation.
Localised swelling, tenderness, or exudate may be apparent.
INVESTIGATIONS
Radiological imaging may confirm deep abscesses.
Meningitis
SIGNS / SYMPTOMS
Meningitis and meningoencephalitis can produce trismus, rigidity, seizures, and opisthotonus, but risus sardonicus is absent.[25]
INVESTIGATIONS
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]
Generalised seizures in children
SIGNS / SYMPTOMS
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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